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Effects of Polysaccharides from Selenium-enriched Pyracantha fortuneana on Mice Liver Injury

机译：富硒火棘多糖对小鼠肝损伤的影响

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We have previously reported that polysaccharides extracted from Pyracantha fortuneana (Maxim.) Li (P. fortuneana) lowered the oxidative stress and inhibited the inflammatory responses in mice. Our present study aims to determine the effects of Selenium enriched P. fortuneana polysaccharides (Se-PFPs) against carbon tetrachloride (CCl4)-induced liver injury in a mouse model. Our results displayed that CCl4 remarkably elevated the levels of alanine transferase (ALT), aspartate transaminase (AST), lactic dehydrogenase (LDH), cholesterol, triglycerides in serum. However, similar to BP treatment, supplementation of mice with Se-PFPs resulted in reversal of ALT, AST, LDH, cholesterol, triglycerides in serum. Contrary to CCl4, supplementation of mice with Se-PFPs elevated the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of glutathione (GSH) in liver. Furthermore, Se-PFPs treatment increased the expression of GPx and catalase (CAT) at mRNA and protein levels in liver which were decreased in CCl4 group. Contrary to CCl4, Se-PFPs supplement decreased the levels of thiobarbituric acid reactive substances (TBAR) and H2O2, which served as lipid peroxidation biomarker. Our study indicates that Se-PFPs administration is effective in attenuating CCl4-induced liver injury. The mechanism underlying this effect may be attributed to the reduction of oxidative stress and inflammation in the liver by Se-PFPs through up-regulation of the antioxidant system. Our study suggests that Se-PFPs might be a potential dietary agent in the prevention of hepatic damage.
机译：我们以前曾报道过，从火棘（Maxim。）Li（P. fortuneana）中提取的多糖降低了小鼠的氧化应激并抑制了炎症反应。我们目前的研究旨在确定富硒的贯叶连翘多糖（Se-PFPs）对四氯化碳（CCl4）诱导的小鼠肝损伤的作用。我们的结果表明，CCl4显着提高了血清中丙氨酸转移酶（ALT），天冬氨酸转氨酶（AST），乳酸脱氢酶（LDH），胆固醇，甘油三酸酯的水平。但是，与BP治疗相似，向小鼠补充Se-PFPs会导致血清中的ALT，AST，LDH，胆固醇，甘油三酸酯逆转。与CCl4相反，向小鼠补充Se-PFPs可提高肝脏中的超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和谷胱甘肽（GSH）的活性。此外，Se-PFPs处理增加了肝脏中mRNA和蛋白质水平的GPx和过氧化氢酶（CAT）的表达，而CCl4组则降低了。与CCl4相反，Se-PFPs补充剂可降低硫代巴比妥酸反应性物质（TBAR）和H2O2的水平，后者是脂质过氧化的生物标志物。我们的研究表明，Se-PFPs给药可有效减轻CCl4诱导的肝损伤。此作用的潜在机制可能归因于Se-PFP通过上调抗氧化剂系统来减轻肝脏中的氧化应激和炎症。我们的研究表明，Se-PFPs可能是预防肝损害的潜在饮食剂。

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