2012PubMedRequires access

Protective effect of alpha-mangostin against type-I collagen formation in thioacetamide-induced cirrhotic rat.

Raksawan Poonkhum, Ramida Watanapokasin, Wisuit Pradidarcheep

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Abstract

OBJECTIVE: To elucidate the protective effect of alpha-mangostin (alpha-MG) against increment of type-I collagen-positive hepatocytes in rat cirrhosis induced by thioacetamide (TAA). MATERIAL AND METHOD: Rats were separated into 4 groups. The first group was, the control, untreated with TAA. The cirrhotic rats, the second group, were induced by TAA injection (200 mg/kg), 3 times per week. Rats in the third group received treatment of TAA (200 mg/kg) alternating with alpha-MG (100 mg/kg) for every other day. Animals in the last group were treated only with alpha-MG (100 mg/kg), 3 times per week. The chemicals used each group were given intraperitoneally for 16 weeks. The type-I collagen and type-I collagen-positive hepatocytes were explored by using immunohistochemical technique. RESULTS: In cirrhotic livers type-I collagen was immunopositive in the connective tissue and a large number of hepatocytes. The number of type I collagen-positive-hepatocytes (414.00 +/- 25.23) in TAA-induced cirrhosis group increased significantly when compared to those in the control group (131.40 + 9.63). Interestingly, a significant decrease in the number of type-I collagen-positive-hepatocytes was observed in TAA-alpha-MG-prevention group (103.60 +/- 36.55) and in alpha-MG-injected group (54.00 +/- 5.30) compared to those in the control group and TAA-induced cirrhosis. CONCLUSION: 100 mg/kg of alpha-MG could lower the number of type-I collagen-positive-hepatocytes in TAA-induced cirrhosis. It is probable that alpha-MG helps to keep up more blood circulation to the liver cells through dilated sinusoids. This vascular adaptation enhances high oxygen blood to the hepatocytes which, in turn, reduces the damage of hepatocytes caused by TAA-derived reactive oxygen species.

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OBJECTIVE: To elucidate the protective effect of alpha-mangostin (alpha-MG) against increment of type-I collagen-positive hepatocytes in rat cirrhosis induced by thioacetamide (TAA). MATERIAL AND METHOD: Rats were separated into 4 groups. The first group was, the control, untreated with TAA. The cirrhotic rats, the second group, were induced by TAA injection (200 mg/kg), 3 times per week. Rats in the third group received treatment of TAA (200 mg/kg) alternating with alpha-MG (100 mg/kg) for every other day. Animals in the last group were treated only with alpha-MG (100 mg/kg), 3 times per week. The chemicals used each group were given intraperitoneally for 16 weeks. The type-I collagen and type-I collagen-positive hepatocytes were explored by using immunohistochemical technique. RESULTS: In cirrhotic livers type-I collagen was immunopositive in the connective tissue and a large number of hepatocytes. The number of type I collagen-positive-hepatocytes (414.00 +/- 25.23) in TAA-induced cirrhosis group increased significantly when compared to those in the control group (131.40 + 9.63). Interestingly, a significant decrease in the number of type-I collagen-positive-hepatocytes was observed in TAA-alpha-MG-prevention group (103.60 +/- 36.55) and in alpha-MG-injected group (54.00 +/- 5.30) compared to those in the control group and TAA-induced cirrhosis. CONCLUSION: 100 mg/kg of alpha-MG could lower the number of type-I collagen-positive-hepatocytes in TAA-induced cirrhosis. It is probable that alpha-MG helps to keep up more blood circulation to the liver cells through dilated sinusoids. This vascular adaptation enhances high oxygen blood to the hepatocytes which, in turn, reduces the damage of hepatocytes caused by TAA-derived reactive oxygen species.

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Available abstract

OBJECTIVE: To elucidate the protective effect of alpha-mangostin (alpha-MG) against increment of type-I collagen-positive hepatocytes in rat cirrhosis induced by thioacetamide (TAA). MATERIAL AND METHOD: Rats were separated into 4 groups. The first group was, the control, untreated with TAA. The cirrhotic rats, the second group, were induced by TAA injection (200 mg/kg), 3 times per week. Rats in the third group received treatment of TAA (200 mg/kg) alternating with alpha-MG (100 mg/kg) for every other day. Animals in the last group were treated only with alpha-MG (100 mg/kg), 3 times per week. The chemicals used each group were given intraperitoneally for 16 weeks. The type-I collagen and type-I collagen-positive hepatocytes were explored by using immunohistochemical technique. RESULTS: In cirrhotic livers type-I collagen was immunopositive in the connective tissue and a large number of hepatocytes. The number of type I collagen-positive-hepatocytes (414.00 +/- 25.23) in TAA-induced cirrhosis group increased significantly when compared to those in the control group (131.40 + 9.63). Interestingly, a significant decrease in the number of type-I collagen-positive-hepatocytes was observed in TAA-alpha-MG-prevention group (103.60 +/- 36.55) and in alpha-MG-injected group (54.00 +/- 5.30) compared to those in the control group and TAA-induced cirrhosis. CONCLUSION: 100 mg/kg of alpha-MG could lower the number of type-I collagen-positive-hepatocytes in TAA-induced cirrhosis. It is probable that alpha-MG helps to keep up more blood circulation to the liver cells through dilated sinusoids. This vascular adaptation enhances high oxygen blood to the hepatocytes which, in turn, reduces the damage of hepatocytes caused by TAA-derived reactive oxygen species.

Key concepts: Thioacetamide, Cirrhosis, Medicine, Alpha (finance), Internal medicine, Connective tissue, Type I collagen, Endocrinology

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Protective effect of alpha-mangostin against type-I collagen formation in thioacetamide-induced cirrhotic rat. — Research Paper | ScholarLens