Anti-lipid peroxidation and protection of liver mitochondria against injuries by picroside Ⅱ

AIM: To investigate the anti-lipid peroxidation and protection of liver mitochondria against injuries in mice with liverdamage by picroside Ⅱ.METHODS: Three animal models of liver damageinduced by carbon tetrachloride (CCl4:0.1 mL/10 g, ip),D-galactosamine (D-GalN: 500 mg/kg,ip) and acetaminophen (AP: 0.15 g/kg, ip) were respectively treated with various concentrations of picroside Ⅱ (5, 10, 20 mg/kg, ig). Then we chose the continuously monitoring method (recommended by International Clinical Chemistry League) to analyze serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values, Marland method to detect the activity of manganese-superoxide dismutase (SOD) in liver mitochondria, TBA colorimetry to determine the content of malonicdialdehyde (MDA) in liver tissue, DTNB method to evaluate the activity of glutathioneperoxidase (GSH-Px) and Lowry method to detect protein level in liver tissue. Meanwhile, effects of picroside Ⅱ on the activity of ATPase and swelling extent of mitochondria in hepatocytes damaged by AP were also evaluated.RESULTS: Picroside Ⅱ could significantly prevent liver toxicity in the three models of liver damage. It decreased the high levels of ALT and AST in serum induced by theadministration of CCl4, D-GalN and AP, reduced the cellular damage of liver markedly, and appeared to be even more potent than the positive control drug of biphenyl dimethyl dicarboxylate pilules (DDB). In groups treated with different doses of picroside Ⅱ, compared to the model group, the content of MDA in serum decreased evidently, whereas the content of SOD and GSH-Px increased in a dosedependent manner, and the difference was statistically significant. Further, in the study of AP model, picroside Ⅱinhibited AP-induced liver toxicity in mice, enhanced the activity of ATPase, improved the swelling extent of mitochondria and helped to maintain a normal balance of energy metabolism.CONCLUSION: Picroside Ⅱ can evidently relieve hepatocyteinjuries induced by CCl4, D-GalN and AP, help scavenge free radicals, protect normal constructions of mitochondria membrane and enhance the activity of ATPase in mitochondria,thereby modulating the balance of liver energy metabolism, which might be part of the mechanisms of hepatoprotectiveeffects of picroside Ⅱ.

AIM: To investigate the anti-lipid peroxidation and protection of liver mitochondria against injuries in mice with liver damage by picroside Ⅱ. METHODS: Three animal models of liver damage induced by carbon tetrachloride (CCl4: 0.1 mL/10 g, ip), D-galactasamine (D-GaIN: 500 mg/kg, ip) and acetaminophen (AP: 0.15 g/kg, ip) were respectively treated with various concentrations of picroside Ⅱ (5, 10, 20 mg/kg, ig). Then we chose the continuously monitoring method (recommended by International Clinical Chemistry League) to analyze serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values, Marland method to detect the activity of manganese-superoxide dismutase (SOD) in liver mitochondria, TBA colorimetry to determine the content of malonicdialdehyde (MDA) in liver tissue, DTNB method to evaluate the activity of glutathioneperoxidase (GSH-Px) and Lowry method to detect protein level in liver tissue. Meanwhile, effects of picroside Ⅱ on the activity of ATPase and swelling extent of mitochondria in hepatocytes damaged by AP were also evaluated. RESULTS: Picroside Ⅱ could significantly prevent liver toxicity in the three models of liver damage. It decreased the high levels of ALT and AST in serum induced by the administration of CCl4, D-GaIN and AP, reduced the cellular damage of liver markedly, and appeared to be even more potent than the positive control drug of biphenyl dimethyl dicarboxylate pilules (DDB). In groups treated with different doses of picroside Ⅱ, compared to the model group, the content of MDA in serum decreased evidently, whereas the content of SOD and GSH-Px increased in a dose dependent manner, and the difference was statistically significant. Further, in the study of AP model, picroside Ⅱ inhibited AP-induced liver toxicity in mice, enhanced the activity of ATPase, improved the swelling extent of mitochondria and helped to maintain a normal balance of energy metabolism. CONCLUSION: Picroside II can evidently relieve hepatocyte injuries induced by CCI4, D-GaIN and AP, help scavenge free radicals, protect normal constructions of mitochondria membrane and enhance the activity of ATPase in mitochondria, thereby modulating the balance of liver energy metabolism, which might be part of the mechanisms of hepatoprotective effects of picroside Ⅱ.