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.

The influence of lanthanum chloride on the TNFalpha expression of murine peritoneal macrophages stimulated by lipopolysaccharide / 中华烧伤杂志

<p><b>OBJECTIVE</b>To explore the influence of lanthanum chloride on the TNFalpha expression of murine peritoneal macrophages stimulated by lipopolysaccharide (LPS).</p><p><b>METHODS</b>Murine peritoneal macrophages (Mphi) were isolated, cultured and then stimulated by LPS. The influence of lanthanum chloride on the TNFalpha secretion and TNFalphamRNA expression of murine Mphi stimulated by LPS was determined by ELISA method and SYBR green fluorescence quantitative RT-PCR. Forty BALB/C mice were randomly divided into two groups and were treated by lethal dose of LPS and lanthanum chloride processed LPS, respectively. The mortality within 7 days was observed.</p><p><b>RESULTS</b>The TNFalpha secretion and TNFalphamRNA expression level of the Mphi from mice treated by lanthanum chloride processed LPS were obviously lower than those by LPS only (P < 0.01). The mortality of the mice treated by lethal dose of LPS which has been processed by lanthanum chloride was significantly lower than that by lethal dose of LPS only.</p><p><b>CONCLUSION</b>Lanthanum chloride possessed the capacity of lowering down the toxicity of LPS and inhibiting the TNFalpha secretion and TNFalphamRNA expression in murine Mphi stimulated by LPS.</p>