Lyciumbarbarum polysaccharides ameliorate canine acute liver injury by reducing oxidative stress, protecting mitochondrial function, and regulating metabolic pathways / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl4). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl4 solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl4-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.

Effects of endotoxin on phospholipid metabolism and membrane fluidity in liver mitochondria of goats / 中国病理生理杂志

AIM and METHOD:To study the changes of contents of phosphatidyl inositol (PtdIns),phosphatidylserine (Ptdser),phosphatidylethanolamine (PtdEtn) and phosphatidylcholine(PtdCho) in hepatic mitochondria membrane of goats in vivo at 5 h after administration of E. coli endotoxin(1800 U/kg body weight) with HPLC. The membrane fluidity of the erythrocyte and liver mitochondria of E. coli endotoxin treated group was examined with the fluorescence polarization technique, in which 1,6-diphenyl-1,3,5,-hexatriene was used as a fluorescence probe. RESULTS: E. coli endotoxin treated group (group II) led to a marked decrease of PtdIns, PtdSer, PtdEtn, PtdCho contents of hepatic mitochondria in vivo at 5 h as compare to the normal control (group I) ( P