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目的研究橙皮苷(HDN)对对乙酰氨基酚(APAP)诱导小鼠急性肝损伤的保护作用。方法 48只雄性BALB/c小鼠随机均分为6组:正常组,模型组,HDN组(浓度分别为500、250、125 mg/kg),联苯双酯组。HDN组分别灌胃不同浓度的HDN悬液,联苯双酯组灌胃等量联苯双酯溶液,正常组和模型组给予等量的0.5%羧甲基纤维素钠溶液,各组1次/d,连续10 d。末次灌胃后禁食不禁水,2 h后除正常组外其余各组腹腔注射APAP(150 mg/kg)溶液建立小鼠急性肝损伤动物模型。16 h后处死小鼠,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)及肝匀浆丙二醛(MDA)、谷胱甘肽(GSH)水平,光学显微镜下观察肝组织病理组织学变化,逆转录-聚合酶链式反应(RTPCR)法和免疫组织化学法测定肝脏高迁移率族蛋白B1(HMGB1)水平。结果 HDN能显著降低小鼠血清ALT、AST、肝匀浆MDA水平,提高肝组织中GSH活性,改善肝组织损伤程度。RT-PCR法和免疫组织化学法显示,HDN可以抑制HMGB1的转录和释放。结论 HDN对APAP诱导小鼠急性肝损伤具有保护作用,可能与其抑制HMGB1 mRNA转录和释放有关。
Objective To study the protective effect of hesperidin (HDN) on acute hepatic injury induced by acetaminophen (APAP) in mice. Methods 48 male BALB / c mice were randomly divided into 6 groups: normal group, model group, HDN group (500,250,125 mg / kg, respectively) and bifendate group. HDN group were given different concentrations of HDN suspension, bifendate group were administered the same amount of bifendate solution, normal group and model group were given the same amount of 0.5% sodium carboxymethyl cellulose solution, each group 1 / d for 10 days. After the last gavage, fasting could not help but water. After 2 h, the mice in the other groups were given APAP (150 mg / kg) solution to establish acute liver injury model in mice. After 16 h, the mice were sacrificed and serum ALT, AST, and liver homogenate malondialdehyde (MDA) and glutathione (GSH) levels were measured. Liver histopathology was observed under light microscope The levels of high mobility group box 1 (HMGB1) in the liver were measured by reverse transcription - polymerase chain reaction (RT - PCR) and immunohistochemistry. Results HDN could significantly reduce the levels of serum ALT, AST and liver homogenate MDA in mice, increase the activity of GSH in liver tissue, and improve the degree of liver injury. RT-PCR and immunohistochemistry showed that HDN could inhibit the transcription and release of HMGB1. Conclusion HDN can protect APAP-induced acute liver injury in mice, which may be related to the inhibition of HMGB1 mRNA transcription and release.