Animal and Human Studies of Tartary Buckwheat

Statements about the health benefits of consuming Tartary buckwheat often rely on a combination of demonstrations: 1) that a certain chemical compound occurs within the plant; 2) that that compound affects others found within the human body (or the bodies of other animals); and 3) that such effects reduce the likelihood of disease and/or improve the prognosis for ill individuals. There are few observational studies or experiments that directly compare the physiological or health status of individuals (animal or human) who consume buckwheat with the status of those who don’t. Nevertheless, the studies below demonstrate a variety of healthful effects achieved by adding Tartary buckwheat to the diet.



It might seem unnecessary to say that consuming a putative “health food” doesn’t harm people; however, a substance that is healthful at one dosage for one person might be harmful at a different dosage or for a different subject (different age, sex, genetic background, or health history). Therefore, a survey of animal studies on the healthful effects of Tartary buckwheat appropriately begins with a study of its possible toxic effects. Lin et al. (2001) investigated the toxicological safety of a powdered extract of Tartary buckwheat. Those authors subjected mice and Wistar rats to a 30-day feeding trial that compared low, medium, and high dosages of the extract with a control diet. Neither males nor females of either species exhibited a significant difference in feed use efficiency or final body weight due to the dietary treatments. In the experimental mice, the types and frequencies of deformations in sperm cells were unaffected by Tartary buckwheat extract in the diet. Nor did the extract affect the frequency of polychromatic erythrocytic micronuclei in the bone marrow of the mice. Blood levels of hemoglobin and the numbers of erythrocytes and leucocytes in male and female rats were similarly unaffected by Tartary buckwheat extract in the diet. The authors also reported blood levels of glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), albumin, total protein, sugar, urea nitrogen, HDL, triglyceride, and cholesterol in the blood of male and female rats. None of these substances was significantly affected by the feeding treatments. The authors reported that the extract had an LD50 greater than 10g/kg, a level considered non-toxic.


Foods that are high in dietary fiber or resistant starch can create a feeling of satiety without elevating serum glucose level or the body’s insulin response.  Berti et al. (2005) examined how consumption of a first course of pasta affects caloric intake during the balance of a meal (ham, cream cheese, crackers, chips, strawberry yoghurt, apricot jam tart, apple, banana, and water).  The pasta dishes examined were regular spaghetti (i.e., wheat flour); spaghetti containing 40% oat flour; regular lasagne (wheat flour, 20% egg); buckwheat lasagne (60% common buckwheat flour, 40% precooked rice flour, 30% egg); and carboxymethyl cellulose/buckwheat lasagne (above recipe augmented with 0.5% CMC).  Fourteen healthy male volunteers (average age of 24.0 years) were assigned in random order a course of 200g of each pasta (dressed with 50g of tomato sauce) and pasta courses of twice those quantities.  Additionally, subjects were fed the same meal with no preceding pasta course.  Quantities of items subsequently consumed ad libitum were weighed, and caloric intakes were calculated.

The authors reported that the small pasta servings contained between 1181 and 1323kJ, and the large servings twice those energy values.  The mean intake of the test meal with no pasta course contained 4547kJ.  When a large serving of regular lasagne, regular spaghetti, or oat spaghetti was added as the opening course, the total caloric intake was increased.  However, when the meal started with a small course of any of these pasta items, the total caloric intake was lower than with no pasta course.  When the meal started with a course of buckwheat lasagne or CMC/buckwheat lasagne—large portion or small—the total caloric intake was lower than with no pasta course.  The authors concluded that the substitution of common buckwheat flour for wheat flour in the preparation of lasagne increased the satiating power of the resultant dish.  The mean palatability score of regular lasagne (6.7) was the highest of all these pasta dishes; whereas the mean palatability score of the buckwheat lasagne (4.1) was the lowest.  As discussed in the section on TARTARY BUCKWHEAT AND NUTRITION, Tartary buckwheat contains dietary fiber and resistant starch at levels equivalent to common buckwheat.  Therefore, pasta containing Tartary buckwheat flour would likely have similar effects as the experimental lasagnes that contained common buckwheat flour (both with and without carboxymethyl cellulose).


Jin and Wei (2011) administered (daily, by gavage) three levels of an ethanol extract of Tartary buckwheat seeds for 28 days to randomized groups of 3-month-old mice. Mice that had received the extract were able to swim significantly longer than control mice that had received none. The duration of swimming was positively related to the amount of extract administered (60, 120, or 240mg per kg body weight). Mice receiving those same treatments were euthanized after 90 minutes of swimming, and levels of lactic acid and urea nitrogen were measured in their blood. The blood from mice receiving the buckwheat extract contained significantly lower levels of both metabolic by-products than the blood of control mice. Moreover, the mice receiving the extract contained significantly higher concentrations of glycogen in both liver and muscle tissue. Those mice also had significantly greater concentrations of glutathione peroxidase and superoxide dismutase in skeletal muscle, with levels of those antioxidant enzymes correlated with the level of buckwheat extract received. According to the authors, the putative mechanism by which Tartary buckwheat delays fatigue is that it slows the rise in blood lactic acid, increases tissue glycogen reserve after exercise, and thereby increases the capacity for aerobic and anaerobic exercise. In addition, Tartary buckwheat is rich in flavonoids; together with endogenous antioxidants these compounds can suppress the reactive oxygen species that contribute strongly to muscle fatigue.


Wieslander et al. (2012) conducted a double-blind experiment on the effect of buckwheat consumption on general and mucosal symptoms in 62 healthy female day-care workers in Sweden. The workers were randomly assigned to two groups fed cookies containing either Tartary or common buckwheat flour. The former represented a daily dosage of 156.6 mg of rutin and 197.8 mg of quercetin; the latter represented a daily dosage of 16.3 mg of rutin and undetectable quercetin. After two weeks the groups were switched to the alternative treatment, which was then administered for two additional weeks. At the experiment’s commencement and after weeks 2 and 4, the subjects were questioned about current ocular, nasal, and throat symptoms, as well as headache, fatigue, and nausea symptoms.
Compared to their baseline scores, the combined experimental groups showed significant improvement in nasal irritation, headache (to week 2), and fatigue (to week 4). These changes might have been due to any of the constituent compounds common to both buckwheat species. During the first treatment period, improvement in ocular irritation was significantly better in the group consuming common buckwheat, whereas the improvement in fatigue was significantly better in the group consuming Tartary buckwheat. The greater concentration of rutin in the Tartary buckwheat cookies was likely responsible for the different changes in fatigue scores in the experimental groups.


Hyperglycemia is the term for elevated levels of glucose circulating in the blood. “Glucose tolerance” is a measure of the body’s ability to respond to a rise in serum glucose, and to transport that glucose into cells. If glucose tolerance is impaired, hyperglycemia persists. Over time this can cause serious secondary symptoms, such as the deterioration of peripheral blood vessels, which in turn can lead to blindness, limb amputations, or even death. Insulin, synthesized by specialized cells within the pancreas, plays a critical role in the transport of glucose from the bloodstream into mammalian cells. Hyperglycemia can result either from the failure of the pancreas to produce insulin (Type 1 diabetes mellitus) or from the failure of the body’s cells to respond to insulin (Type 2 diabetes mellitus).
As mentioned in the section on SOLUBLE CARBOHYDRATES in NUTRITIONAL ASPECTS OF TARTARY BUCKWHEAT, buckwheat is one of the best plant sources of D-chiro-inositol (D-CI). D-chiro-inositol can be a component of yet larger molecules that are involved in the cellular uptake of serum glucose. Those compounds act effectively as insulin mimics or substitutes. Streptozotocin (STZ) is a toxin to the insulin-producing cells of the pancreas. A single large dose of STZ can be used in an animal model to induce hyperglycemia. In multiple lower doses, STZ can be used to simulate either Type 1 or Type 2 diabetes. Therefore, streptozotocin-treated rats have been used to evaluate the effectiveness of D-chiro-inositol as a replacement for or supplement to the body’s insulin production.

An intragastric dose of D-chiro-inositol to STZ-treated rats has been shown to diminish the rise in the level of serum glucose that follows an intraperitoneal administration of glucose. Kawa et al. (2003) noted that buckwheat seeds offer a natural dietary source of D-CI that could potentially counteract hyperglycemia. Those authors evaluated the effect of an acute dose of a buckwheat extract concentrate on glucose tolerance in normal rats, and also its effect on elevated serum glucose in fed STZ-treated rats.

An ethanol extract was prepared from the combined “shorts” and “bran” fractions from milled, dehulled groats of ‘Koto’ common buckwheat. The concentrate comprised 0.2% D-CI , 0.1% myo-inositol, 5.7% fagopyritols, and 6.0% sucrose. Following 7 days of acclimation, normal male rats (150-180 g) were given a dose of buckwheat concentrate corresponding to 10 mg of D-CI per kg body weight. A sucrose solution was administered to control rats. After a two-hour fast, glucose (4 g/kg body weight) was administered to those rats intraperitoneally. At subsequent 30 minute intervals, venous blood was drawn and sampled for glucose. For rats receiving either the dose of buckwheat concentrate or the control solution, serum glucose peaked at 30 minutes, at which time the former was significantly lower (-17%) than the latter. The buckwheat extract had improved the glucose tolerance of normal rats.

Kawa et al. (2003) also administered the buckwheat concentrate (10 or 20 mg of D-CI per kg body weight) to rats in which diabetes had been induced by prior intraperitoneal injections of STZ. In the diabetic rats that received the lower dose of buckwheat concentrate, subsequent serum glucose levels declined (significantly so at 60 minutes and subsequently). In the diabetic rats that received the higher concentration of buckwheat extract, after 90 minutes the serum glucose had declined from its initial level. In contrast, in control diabetic rats the concentration of serum glucose did not drop significantly over the two hours following administration of the sucrose placebo. The observed effects of the buckwheat extract were similar in magnitude to those reported when chemically-synthesized D-CI had been administered to rats in which diabetes had been induced with STZ.

Kawa et al. (2003) also performed an Oral Glucose Tolerance Test to fasting rats in which diabetes had been induced with STZ. The investigators administered buckwheat extract concentrate intragastrically to STZ rats following a 4-hour fast. One hour later, blood was sampled intravenously, and the rats then received 1 g glucose per kg body weigh (in 70% solution, intragastrically). Intravenous blood samples at subsequent 30-minute intervals revealed a rise in serum glucose at 30 minutes and then a decline over the following 90 minutes. Glucose levels were consistently lower in the rats receiving the buckwheat concentrate (at either dosage) than in the corresponding controls; however, these differences were not statistically significant.

While the authors speculated that the observed effects of buckwheat were caused by its constituent D-chiro-inositol, the means by which serum glucose levels were reduced remain unknown. The anti-hyperglycemic effect of D-CI may result from inhibition of hepatic glucose output or by stimulation of glycogen synthesis; by enhanced glucose transport; or by increased glucose utilization or disposal.

As detailed in the section on TARTARY BUCKWHEAT FUNCTIONAL FOODS, Yao et al. (2008) produced an extract of Tartary buckwheat bran that was enriched in free D-chiro-inositol (D-CI). Bran (containing tissue of both the seed coat and the embryo) contains relatively high levels of both D-CI and fagopyritols. Bran was extracted with 60 percent ethanol, and concentrated under reduced pressure. Steaming of this bran extract under pressure apparently hydrolyzed the constituent fagopyritols. Subsequent column chromatography with activated charcoal and ion exchange resins increased the free D-CI concentration to 22 percent.

Yao et al. (2008) tested the oral toxicity of this purified Tartary buckwheat bran extract, administering 20g of extract daily per kg body weight of ICR mice. After 14 days, none of the 20 treated mice had died, all were generally healthy, and body weights were not significantly different from those of control mice.

KK-Ay mice carry a homozygous mutation that causes metabolic abnormalities such as hyperglycemia and glucose intolerance—phenotypically similar to human type 2 diabetes. Yao et al. (2008) fed KK-Ay mice a ration that included 0 (control), 45, 91, or 182 mg of Tartary buckwheat bran extract per kg. After five weeks, these mice were tested for oral glucose tolerance. After fasting overnight, mice receiving all three experimental treatments had lower serum glucose levels than control (diabetic) mice. Dose-dependent differences in the glucose level were also observed 30, 60, and 120 minutes after these mice had received a dose of glucose equivalent to 2 g per kg body weight. Compared to the control diabetic mice, those receiving rations containing bran extract exhibited generally lower plasma levels of C-peptide, glucagon, BUN, triglycerides, and total cholesterol. At the highest treatment level (equivalent to 40 mg D-CI per kg) the decreases in all but the last were statistically significant.

D-chiro-inositol is not the only constituent of Tartary buckwheat that might protect against diabetes. Li et al. (2016) studied the hypoglycemic and hypolipidemic effects in rats of a flavonoid-rich extract from Tartary buckwheat seeds. The ethanol-water (60:40) extract from powdered seeds was subjected to microwaves (600W) at 70°C for 20 minutes, then centrifuged, filtered, and the filtrate evaporated. In the solid product the total flavonoids constituted 27.97mg/g.

To fasting male rats that had been fed a high-fat (45% fat) diet for four weeks, the researchers administered intraperitoneally STZ at a dose of 60mg/kg body weight. Seventy-two hours later, venous blood was drawn and rats were divided into a diabetic control group; low-, middle-, or high-dose Tartary buckwheat treatments (100, 200, and 400mg/kg, respectively); and a group treated with a glibenclamide solution (4mg/kg). Besides those groups, all of which were fed a high-fat diet for 28 days, there was a normal control group maintained on a diet containing 12% fat. Following an overnight fast, venous blood was drawn from the rats in all groups once a week.

Li and co-workers reported that compared to the normal control group, fasting blood glucose levels were initially elevated in all the (diabetic) treatment groups. However, at 14 days glucose levels were significantly lower in all three Tartary buckwheat treatments and the glibenclamide treatment, compared to the diabetic control group. Despite a progressive and dose-dependent response, after 28 days mean glucose levels in all the treatment groups remained significantly higher than in the normal control rats. Similarly, the serum insulin levels were significantly lower in the Tartary buckwheat and glibenclamide groups than in the diabetic control group, as were serum lipid levels (TC, TG, and LDL-C). Conversely, HDL-C levels were significantly higher in those groups than in the diabetic controls.

The investigators conducted an oral glucose tolerance test on the 28th day, with serum glucose measured at 0, 30, 60, and 90 minutes after glucose was administered. For all the treatment groups, serum glucose levels were intermediate between those in the normal control rats and the diabetic control rats, with glucose levels peaking at 30 minutes in all groups.

These results indicate that consumption of a Tartary buckwheat extract containing almost 3 percent total flavonoids can reduce STZ-induced hyperglycemia in rats. An oral glucose tolerance test demonstrated that the extract can improve blood glucose homeostasis, and control the hyperinsulinemia by which the body compensates for high serum levels of glucose. Moreover, the extract countered the abnormal concentration of serum lipids that in diabetics can result from the mobilization of fats from adipose tissue.


Because high levels of serum cholesterol (particularly LDL) are associated with the risk of cardiovascular disease, many studies have explored dietary factors that might lower levels of cholesterol in the blood.  As discussed in the section “BUCKWHEAT AND CHOLESTEROL,” protein in buckwheat flour, once digested, can bind with bile salts.  By promoting the excretion of bile salts via the feces, buckwheat protein digests might diminish their recycling via the enterohepatic circulation.  Because buckwheat contains substantial amounts of flavonoids, and because the presence of these compounds has been shown to affect serum lipid levels, these compounds constitute another avenue by which buckwheat could protect against cardiovascular disease.

In their study of Swedish day-care workers discussed above, Wieslander et al. (2011) also studied possible effects of buckwheat consumption on lung function, dyspnoea, and markers related to cardiovascular disease. Compared to their baseline scores, the combined experimental groups showed significant reductions in total serum cholesterol and HDL cholesterol (after 4 weeks). Of various measures of lung function, only Forced Vital Capacity showed significant improvement (at 4 weeks). Three markers of inflammation—-levels of serum myeloperoxidase (MPO), serum eosinophilic cationic protein (ECP), and nitrous oxide in exhaled blood (NO)-—were not significantly affected by buckwheat consumption. When changes in the high-rutin (Tartary buckwheat cookie) treatment were compared with those in the low-rutin (common buckwheat cookie) treatments, the decline in the serum concentration of myeloperoxide in the former group was significantly greater than in the latter group (at week 4). Moreover, a generalized least-squares model of log-transformed scores for serum MPO showed a substantial negative effect from consumption of Tartary buckwheat. Since MPO is an indicator of neutrophilic inflammation, its reduction implies that rutin has an anti-inflammatory effect.

Lee et al. (2010) investigated the hypolipidemic (cholesterol-lowering) effect of common buckwheat leaves and flowers when added to a high-fat diet.  Leaves and flower parts of common buckwheat grown in Daejon, Korea were air-dried and powdered to pass through a 60-mesh sieve.  For six weeks, groups of male rats (N=10) were fed ad libidum a normal control diet, high-fat diet, or high-fat diet supplemented with buckwheat powder (5% by weight).  Energy content of these diets were 386.2, 498.7, and 501.1 kcal/100g, respectively.  The rats in the high-fat diet had significantly higher energy intake and body weight gain than those in the control group or the group whose high-fat diet was supplemented with buckwheat powder.  The two high-fat groups had identical feed efficiency ratios—significantly higher than that of the control.  In relation to body weight, the liver, heart, and kidney of the rats fed buckwheat powder were significantly smaller than those of the other groups.  The combined weights of adipose tissues (epididymal, perirenal, and interscapular) were lowest in the control group and highest in high-fat diet without buckwheat.

Lee and co-workers (2010) found that the addition of buckwheat powder lowered total plasma cholesterol by 35.9 percent compared to the high-fat diet, and 29.1 percent compared to the control diet.  Total plasma triglycerides were 26.2 percent lower in the buckwheat-augmented diet compared to the high-fat diet, and 34.2 percent lower compared to the control.  Although plasma HDL cholesterol concentration was lowest in the group whose diet included buckwheat powder, the ratio of HDL to total cholesterol was higher in that group than in the group fed a high-fat diet without buckwheat (and equivalent to the control group).  For rats fed a high-fat diet (49.6% of total caloric intake from fats), the addition of buckwheat powder significantly lowered the Atherogenic Index. This index, an estimate of the risk  of cardiovascular disease, was similar to that observed in rats fed a low-fat diet (11.7% of total calories from fat).

Concentrations of triglycerides, cholesterol, and acidic sterol were all higher in feces from the buckwheat-fed rats than from rats on either the control or high-fat diet; the differences in triglyceride and acidic sterol level were significant (p<0.05).

The researchers also isolated hepatic microsomes from rats subjected to the three diets, and assayed these for activity of 3-Hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase and acyl-CoA:cholesterol acyltransferase (ACAT).  The activity of both enzymes was significantly greater in the buckwheat-supplemented diet than in either the control or the high-fat diet.  The authors speculated that the plasma cholesterol reduction effected by the buckwheat powder upregulated HMG-CoA reductase and ACAT as a homeostatic response.


Kuwabara et al. (2007) examined the effects of buckwheat sprouts on the plasma cholesterol concentration, fecal steroid excretion, and hepatic mRNA expression related to cholesterol metabolism in rats. Seeds of one variety of common buckwheat (‘Kitawasesoba’) and two of Tartary buckwheat (‘Hokkai T8’ and ‘Hokkai T9’) that had been harvested in Hokkaido, Japan were germinated in the dark and then grown for 5 days in the light at 22ºC. Leaves and stems were harvested at day 9 (common buckwheat) or day 10 (Tartary buckwheat), weighed, and freeze-dried, and ground. The authors randomly assigned 8-week-old male rats to four groups (n=5). Treatments were cholesterol-free diets augmented 5 percent (w/w) with sprout powder from one of the buckwheat varieties, or 5 percent with ⍺-cornstarch (control). Diets augmented with sprout powder from ‘Kitawasesoba,’ ‘Hokkai T8,’ and ‘Hokkai T9’ contained rutin concentrations of 17, 160 and 213 mg/kg body weight/ d, respectively. Fecal excretion was collected for 3 days at the end of the 4-week treatment, and blood was collected from fasting rats. Diets were resumed for 24 hours prior to the rats being sacrificed for the collection of livers, ceca, and blood.

Feed intake, gain in body weight, and final fresh weight of liver and cecum did not vary significantly among the treatments. Compared to the control group, the groups whose feed was supplemented with sprout powder from ‘Kitawasesoba’ common buckwheat or from ‘Hokkai T8’ Tartary buckwheat exhibited significantly higher fecal matter excretion (dry weight basis). Among the four groups there was no significant difference in plasma levels of triglycerides, HDL cholesterol, or non-HDL cholesterol. Plasma levels of total cholesterol were significantly lower in the groups receiving Tartary buckwheat powder compared to the control group (1.87 and 1.93 mmol/L versus 2.30 mmol/L). Moreover, total cholesterol was significantly lower in the group consuming ‘Hokkai T8’ sprout powder compared to the group consuming the common buckwheat powder (2.20 mmol/L).

Kuwabara et al. (2007) found that the level of cholesterol in liver tissue was higher in the rats on the control diet than on those on any of the diets containing buckwheat sprout powder. The level of cholesterol in feces was lower in rats on the control diet, compared to those on the buckwheat diets. A similar pattern was observed in the fecal levels of coprostanol and of total neutral steroids. None of these contrasts was significant at p<0.05. Levels of individual bile acids (cholic acid, deoxycholic acid, chenodeoxycolic acid, and lithocholic acid) and their total concentration were consistently lower in the feces of the control rats than in the feces of rats consuming buckwheat sprout powders. While some of those differences were significant, there was no significant difference between the level of any bile acid in feces from rats consuming common versus Tartary buckwheat sprout powder. A similar pattern was observed for cecal concentrations of short chain fatty acids (acetate, propionate, and n-butyrate), that is, levels were lower in control rats compared to those consuming buckwheat sprout powder. The authors observed that the addition of buckwheat sprout powder promoted cecal fermentation processes in the rats.

Those authors extracted total hepatic mRNA from the experimental rats. Semi-quantitative RT-PCR amplification, and the subsequent hybridization of PCR products with the respective inner oligonucleotides were used to measure the expression of genes for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and cholesterol 7 ⍺-hydroxylase. Significantly higher levels of mRNA for both genes were found in livers from rats fed ‘Hokkai T9’ Tartary buckwheat sprout powder than in livers of control rats. Higher levels of mRNA of both genes were found in rats fed ‘Hokkai T8’ Tartary or ‘Kitawasesoba’ common buckwheat sprout powder than in livers of control rats; however, these differences were significant only for cholesterol 7 ⍺-hydroxylase. The authors suggested that stimulation of hepatic bile acid synthesis from cholesterol might be a mechanism by which buckwheat sprout powders decreased plasma concentrations of cholesterol.


Merendino et al. (2014) studied oxidative status and blood pressure in hypertensive rats fed pasta that contained Tartary buckwheat sprouts. (Production of sprouts and pasta are described in FUNCTIONAL FOODS section. ) The researchers measured several markers of cardiovascular function in spontaneously-hypertensive and normotensive (WKY) 12-week-old male rats fed diets that included either commercial all-durum pasta or pasta enriched with Tartary buckwheat powdered sprouts. Rats were sacrificed after six weeks on the experimental diets, and plasma total antioxidant capacity was determined by DPPH radical scavenging and by oxygen radical absorbance capacity (ORAC). In both the normatensive and spontaneously-hypertensive rats, both assays for antioxidant capacity showed significantly greater capacity in those rats fed the Tartary buckwheat-enriched diets. Those rats also showed significantly improved plasmatic oxidative response—as indicated by lower plasma levels of protein carbonyl and of malondialdehyde (MDA). The hypertensive rats that had been fed the buckwheat-enhanced diet showed significantly higher levels of endogenous vasodilators (bradykinin and NO metabolite) and a lower level of a vasoconstrictor (endothelin-1).

Merendino et al. (2014) noted, “It is important to note that the levels of blood pressure-related biochemical parameters in the normotensive control rats did not change significantly, which indicates that TBSP [Tartary buckwheat sprout powder] does not have any contraindications for a healthy group of animals.”


Kim et al. (2007) investigated the ability of various extracts from hulls of common buckwheat to kill the cells of several different lines of human cancers. A 70 percent ethanol extract from hulls was sequentially fractionated with n-hexane, chloroform, ethyl acetate, ethanol, and water. An in vitro cell proliferation assay of each fraction tested its cytotoxic effect against each of these human cell lines: A549 lung carcinoma, MCF-7 breast cancer, AGS stomach adenocarcinoma, HeLa cervical adenocarcinoma, and Hep3B hepatocellular carcinoma. Each hull extract fraction was also tested against each of 293 lines of adenovirus-transformed primary human embryonic kidney cells—considered to have more normal characteristics than cancer cells.

The proliferation of human breast adenoid carcinoma (MCF-7) cells was inhibited in a dose-dependent manner by all the hull extracts at concentrations between 0.25 and 1.00 mg/mL; at the highest concentration, inhibition was at least 60 percent. Extracts in ethyl acetate, hexane, and chloroform tended to have the greatest effect. The authors reported similar results with A549 lung carcinoma, Hep3B hepatocellular carcinoma, AGS stomach adenocarcinoma, and HeLa cervical adenocarcinoma cell lines. Lower levels of inhibition were observed in the embryonic kidney cell lines—under 40 percent even at the highest concentration.
The authors sought to verify these anti-tumor properties in an animal model.

To initiate the formation of solid tumors in mice, Kim et al. (2007) transplanted seven-day-old sarcoma-180 cells subcutaneously into the groin of the mice at a dose of 1.0X106 cells per mouse. Beginning 24 hours after sarcoma transplantation, the buckwheat hull extract fractions, at doses of 25 or 50 mg/kg body weight, were injected intraperitioneally daily for 20 days. The control mice were injected with a 0.9% NaCl solution. After 26 days, the resultant tumors were dissected and weighed. Compared to the control group, mice receiving all of the fractions of buckwheat hull extract had tumors of significantly-smaller weight. At the lower dosage, tumor weight was reduced between 11.97 percent (aqueous fraction) and 33.34 percent (ethyl acetate fraction). At the higher dosage, tumor weight was reduced between 31.35 percent (aqueous fraction) and 51.99 percent (ethyl acetate fraction). While Kim and co-authors could not attribute the anti-cancer activity of the extracts to particular chemical constituents, they suggested that buckwheat hull, an inexpensive waste product, could be used in functional foods or pharmaceutical mixtures.


Ishii et al. (2008) investigated the effect of an ethanol extract of powdered sprouts of common buckwheat on inflammation caused by lipopolysaccharide (LPS). LPS is a component of the cell walls of gram-negative bacteria, capable of eliciting a massive response from some phagocytes and macrophages of a host’s immune system. The chemokine, Interleukin-8, and the cytokine, Tumor Necrosis Factor alpha (TNF-⍺), are mediators of this potentially-fatal inflammatory response. Antioxidant compounds, such as the flavonoids found in buckwheat, can disrupt the signaling pathway that leads to inflammation, thereby offering some protection against septic shock. These authors tested the effects of the sprout extract and various purified flavonoid compounds on the expression of an interleukin gene (IL-8) in cultured human colon cancer cell lines that had been exposed to LPS. The secretion of IL-8 from the exposed cells was significantly reduced in the presence of the buckwheat extract. Applied individually, none of the purified flavonoids—vitexin, isovitexin, orientin, isoorientin, keracyanin, chlorogenic acid, or rutin—was as effective as the sprout extract in reducing the expression of the IL-8 gene (even at a concentration twice that measured in the sprout extract). The authors passed the buckwheat extract through a column containing a resin to which most flavonoids fail to bind, and they measured the inflamation-inhibiting potential of the fraction that had passed through that column. They then eluted the fraction that had been retained by the resin, and measured the inflamation-inhibiting potential of that fraction. The authors found that the fraction passing through the column had less anti-inflammatory activity than the fraction that was retained by the column. Thus, the inhibition of the IL-8 gene appeared to be caused by some unknown component of the buckwheat sprout other than the flavonoids. Because the most active compound in the sprout extract was unidentified, its concentration—and even its presence—in a corresponding extract from Tartary buckwheat sprouts cannot be inferred.

Ishii et al. (2008) also measured the expression of TNF-⍺ and IL-6 genes in the spleens and livers of LPS-induced mice, to which common buckwheat sprout extract had been administered orally by gavage. In both organs, mRNAs for both genes were significantly reduced (p<0.05) by administration of the buckwheat extract four hours prior to the sacrifice of 8-week-old female mice. Serum levels of these two cytokines were similarly depressed in mice that had received sprout extract, compared to mice that had been exposed to LPS but no extract.

HeLa (human cervical adenocarcinoma) cells can produce high levels of IL-6 and IL-8 without induction by LPS. Therefore, suppression of those genes by buckwheat sprout extract would demonstrate that its anti-inflammatory effect was due to its direct action on those genes, rather than by blocking the binding of LPS to TLR4. The authors found that genes for both IL-6 and IL-8 were suppressed by extract of common buckwheat sprouts.