Protective Effects ofAtractylodes macrocephalaPolysaccharide on Liver Ischemia–Reperfusion Injury and Its Possible Mechanism in Rats

丙二醛 超氧化物歧化酶 再灌注损伤 抗氧化剂 医学 内分泌学 肝损伤 胆红素 内科学 脂质过氧化 药理学 肝功能 氧化应激 化学 缺血 生物化学
作者
Cheng Jin,Peijian Zhang,Chuanqing Bao,Yuanlong Gu,Binghua Xu,Cheng-Wan Li,Jianping Li,Bo Ping,Xinnong Liu
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:39 (03): 489-502 被引量:24
标识
DOI:10.1142/s0192415x11008981
摘要

Atractylodes macrocephala polysaccharide (AMP), a traditional Chinese medicine, is thought to have protective effects against liver injury. Therefore, this study was designed to explore the effects of AMP on hepatic ischemia–reperfusion injury (IRI) and elucidate the possible mechanisms. Ninety-six Sprague-Dawley rats were randomly divided into four groups with 24 rats per group: a normal control group, an IRI group, an AMP-treated group (0.4 g/kg/d) and a bifendate-treated group (100 mg/kg). Rats were treated with AMP or bifendate once daily for seven days by gastric gavage. The normal control group and the IRI model group received an equivalent volume of physiological saline. At 1, 6 and 24 h after surgery, the rats were killed and liver tissue samples were obtained to determine interleukin-1 (IL-1) expression by Western blotting and nuclear factor-κB (NF-κB) expression by immunohistochemistry. Liver morphology was assessed by microscopy and transmission electron microscopy. Blood samples were obtained to measure liver function (alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin). AMP significantly reduced the elevated expression of markers of liver dysfunction and the hepatic morphologic changes induced by hepatic IRI in rats. AMP also markedly inhibited IRI-induced lipid peroxidation and altered the activities of the antioxidant enzyme superoxide dismutase and malondialdehyde levels. Moreover, pretreatment with AMP suppressed the expression of interleukin-1β and NF-kB in IRI-treated rats. These results suggest that AMP exerts protective and therapeutic effects against hepatic IRI in rats, which might be associated with its antioxidant properties and inhibition of NF-κB activation. More studies are needed to better understand the mechanisms underlying the protective effects of AMP on hepatic IRI.
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