Silymarin-treated Group Research Articles

Effect of Silymarin on Metabolic Factors of Food-Restricted Over Conditioned Wistar Rats

This study was conducted to evaluate the changes in serum metabolic factors of over conditioned pregnant rats treated with silymarin in food restriction condition. Sixty pregnant Wistar rats were divided into five equal groups. All rats received high energy diet before treatments. Control group were fed ad libitum (Non-FR). Rats in other groups received 50% of the food intake of Non-FR group and served as food-restricted (FR) groups. Three of five FR groups received 150, 200 and 400 mg kg(-1) silymarin, respectively (FR-150, 200, 400). Another FR group (FR-Con) and the Non-FR group did not receive any silymarin. Glucose, triglyceride, LDL and HDL cholesterol, total cholesterol, thyroid hormones and cortisol were measured in serum. All factors were significantly different between groups except free-T4 and T4. Serum glucose concentrations in FR-150 and 200 and Non-FR groups were lower than FR-Con and FR-400. Silymarin significantly increased serum triglycerides, LDL cholesterol and cholesterol contents in FR groups. The highest levels of these factors were noted in 200 mg silymarin-treated group. HDL cholesterol was highest in FR-Con; meanwhile FR-200 group had the lowest HDL cholesterol. Serum cortisol decreased in treated and untreated FR groups except FR-150 group. Free-T3 and T3 concentrations in FR-400 and FR-Con groups were higher than the other silymarin treated groups. In conclusion our results indicate that 200 mg kg(-1) of silymarin in Wistar rats is the best dosage to achieve metabolic benefits. Silymarin has positive effects on lipid metabolism and can modulate serum triglyceride and cholesterol concentrations in food restriction condition. Also, the present findings suggest that silymarin under food restriction situation exerts a decreasing effect upon peripheral conversion of T4 to T3.

Protective Effects of Cuscutae semen against Dimethylnitrosamine-Induced Acute Liver Injury in Sprague-Dawley Rats

We investigated the protective effect of Cuscutae semen (CS) on acute liver injury induced by dimethylnitrosamine (DMN) in Sprague-Dawley rats. CS is an important traditional herbal medicine widely used as a tonic and aphrodisiac to nourish the liver and kidney and to treat impotence and seminal emission. Rats were given a single intraperitoneal injection of DMN (40 mg/kg), and were then treated with CS daily by oral gavage for 4 d. Immunohistochemical studies for alpha-smooth muscle actin (alpha-SMA) and proliferating cell nuclear antigen (PCNA) were performed, along with hydroxyproline and biological assay. Liver injury caused by DMN-injection was significantly inhibited in the CS-treated group compared to the silymarin-treated group. The results of blood biological assay were significantly protected by CS in serum total protein (T-protein), T-bilirubin (T-bili), D-bilirubin (D-bili), GOT, GPT, and ALP. The hydroxyproline content and amount of active alpha-SMA and PCNA were significantly decreased in the CS-treated group than in the silymarin-treated group. CS exhibited an in vivo hepatoprotective effect and anti-fibrogenic effects against DMN-induced acute liver injury and inhibited the formation of hydroxyproline, which suggests that CS may be useful in preventing fibrogenesis after liver injury.

장수풍뎅이 유충 추출물이 사염화탄소에 의한 마우스의 간 손상에 미치는 영향

This study was conducted to investigate the effect of methanol extract of Allomyrina dichotoma larva (MEAL) on carbon tetrachloride (CCl4)-induced hepatotoxicity in mice. ICR mice were divided into 5 groups [Vehicle control, CCl4 (10 μg/g) alone, CCl4 plus a low dose (50 μg/g) of MEAL, CCl4 plus a high dose (100 μg/g) of MEAL]. Silymarin (2 μg/g) was used as the reference in the experiment. Administration of MEAL tended to decrease the serum alanine transaminase (ALT) activity induced by CCl4 treatment in mice. Hepatic concentration of thiobarbituric acid-reactive substances (TBARS) in a high-dose group of diet decreased to the level of silymarin-treated group. Hepatic activity of glutathione S-transferase in MEAL-treated group was lower than that of CCl4-treated group. Serum concentration of bilirubin was significantly increased by CCl4 treatment, but MEAL or silymarin recovered the level. These results suggest that MEAL may exert the protective effect against CCl4-induced hepatotoxicity in mice. However, more intensive studies would be needed to elucidate the protective mechanism of the beetle on hepatotoxicity of mice.

Alterations of mast cells and TGF-β1 on the silymarin treatment for CCl4-induced hepatic fibrosis

Silymarin is a potent antioxidant, antiinflammatory and anti-fibrogenic agent in the liver, which is mediated by alteration of hepatic Kupffer cell function, lipid peroxidation, and collagen production. Especially, in hepatic fibrogenesis, mast cells are expressed in chronic inflammatory conditions, and promote fibroblast growth and stimulate production of the extracellular matrix by hepatic stellate cells. We examined the inhibitory mechanism of silymarin on CCl(4)-induced hepatic cirrhosis in rats. At 4, 8, and 12 wk, liver tissues were examined histopathologically for fibrotic changes produced by silymarin treatment. In the silymarin with CCl(4)-treated group, increase of hepatic stellate cells and TGF-beta1 production were lower than in the CCl(4)-treated group at early stages. Additionally, at the late fibrogenic stage, expressions of TGF-beta1 were weaker and especially not expressed in hepatocytes located in peripheral areas. Moreover, the number of mast cell in portal areas gradually increased and was dependent on the fibrogenic stage, but those of CCl(1)+silymarin-treated group decreased significantly. Anti-fibrotic and antiinflammatory effects of silymarin were associated with activation of hepatic stellate cells through the expression of TGF-beta1 and stabilization of mast cells. These results suggest that silymarin prevent hepatic fibrosis through suppression of inflammation and hypoxia in the hepatic fibrogenesis.

Protective effect of silymarin on rat liver injury induced by ischemia.

The effect of silymarin on liver cell damage induced by ischemia was studied in rats fasted for 24 h. In the first series of experiments in vitro ischemia was induced by storing tissue blocks in closed vials at 37 degrees C for 15, 30, 45 and 60 min. Cell injury was detected by the cytophotometrical measurement of glycogen phosphorylase activity in unfixed cryostat sections demonstrated by a modified histochemical procedure. In the second series of experiments in vivo ischemia was provoked by clamping the afferent vessels to the median and left lateral lobes of the liver for 60 min, followed by removal of the clamp and reperfusion. The extent of cell damage was determined by measuring the ALAT and ASAT activities in serum at 1, 3, 6 and 24 h after ischemia and by quantifying the extent of necrosis in the liver after 24 h reperfusion by measuring the unstained areas in cryostat sections incubated for lactate dehydrogenase activity. Silymarin (100 mg/kg b.w.) was administered intravenously at 5 min before both the induction of ischemia and the restoration of blood flow (in vivo ischemia) and at 1 h and at 5 min before sacrifice (in vitro ischemia). Controls received an equal amount of saline. The serum amino-transferase activities after 24 h reperfusion were significantly reduced in the silymarin-treated group (n = 10); ALAT 293 +/- 193 U/L, ASAT 343 +/- 229 U/L compared with the control group (n = 7): ALAT 1238 +/- 743 U/L, ASAT 948 +/- 541 U/L (p < 0.03), and the extent of necrosis decreased from 25.6 +/- 16.0% ( n = 7) to 7.8 +/- 8.3% (n = 10) (p < 0.01) after treatment with silymarin.(ABSTRACT TRUNCATED AT 250 WORDS)