실크 단백질 가수분해물의 간 손상에 대한 보호효과
Protective effect of silk protein hydrolysates against tert-BHP induced liver damage
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초록
The aim of this study was to investigate the hepatoprotecive effect of silk protein hydrolysates (SDH), which was prepared by acid hydrolysis, in rats. SDH itself did not exhibit any cytotoxic effect on hepatic tissues. SDH showed a protective effect on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. SDH effectively reduced AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are biomarkers for liver damage, in a dose-dependent manner. Malondialdehyde (MDA), a lipid peroxidation product, was significantly reduced by SDH. A high dose of SDH (2 g/kg) reduced t-BHP-induced MDA production by 40%. Glutathione (GSH), which is an endogenous antioxidant molecule, was effectively increased by SDH treatment. GSH content was enhanced by around 2.5-fold, compared with t-BHP control, upon SDH (2 g/kg) treatment. Lactate dehydrogenase (LDH), which is an enzyme released by cell cytotoxicity, was greatly increased by t-BHP, but significantly decreased by SDH treatment. Furthermore, hematoxylin and eosin (H&E) staining showed that SDH suppressed t-BHP-induced lesions in liver tissue. Taken together, SDH might be used as a protective agent against liver damage.
Abstract
The aim of this study was to investigate the hepatoprotecive effect of silk protein hydrolysates (SDH), which was prepared by acid hydrolysis, in rats. SDH itself did not exhibit any cytotoxic effect on hepatic tissues. SDH showed a protective effect on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. SDH effectively reduced AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are biomarkers for liver damage, in a dose-dependent manner. Malondialdehyde (MDA), a lipid peroxidation product, was significantly reduced by SDH. A high dose of SDH (2 g/kg) reduced t-BHP-induced MDA production by 40%. Glutathione (GSH), which is an endogenous antioxidant molecule, was effectively increased by SDH treatment. GSH content was enhanced by around 2.5-fold, compared with t-BHP control, upon SDH (2 g/kg) treatment. Lactate dehydrogenase (LDH), which is an enzyme released by cell cytotoxicity, was greatly increased by t-BHP, but significantly decreased by SDH treatment. Furthermore, hematoxylin and eosin (H&E) staining showed that SDH suppressed t-BHP-induced lesions in liver tissue. Taken together, SDH might be used as a protective agent against liver damage.
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