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目的探讨山奈酚对D-氨基半乳糖(D-Ga IN)/脂多糖(LPS)诱导小鼠急性肝衰竭(acute hepatic failure,AHF)的干预作用。方法 37只C57 BL/6小鼠按完全随机分组法分为正常对照组(10只)、AHF模型组(13只)、山奈酚干预组(14只)。AHF模型组小鼠腹腔注射D-Ga IN(700 mg/kg)/LPS(10μg/kg),作用6 h,建立AHF模型;山奈酚干预组小鼠于建模前2 h尾静脉注射5 mg/kg的山奈酚,后腹腔注射D-Ga IN(700 mg/kg)/LPS(10μg/kg),作用6 h,建立AHF模型。正常对照组腹腔注射等量生理盐水。检测血清ALT、AST水平,观察肝脏组织病理学变化,检测肝脏组织中炎症因子TNF-α、IL-1β、IL-6 mRNA表达,检测NF-κB通路相关分子表达及肝细胞凋亡情况。结果与AHF模型组比较,山奈酚干预组小鼠的生存率提高(P<0.05)。与正常对照组比较,AHF模型组血清ALT和AST水平升高(P<0.05),炎症因子TNF-α、IL-1β、IL-6 mRNA表达升高(P<0.05),肝脏组织中NF-κB信号通路相关分子IκB-α表达降低(P<0.05),p-NF-κBp65表达升高(P<0.05),肝脏病理损伤严重,细胞凋亡增多;与AHF模型组比较,山奈酚干预组血清ALT和AST水平降低(P<0.05),炎症因子TNF-α、IL-1β和IL-6 mRNA表达降低(P<0.05),肝脏组织中NF-κB信号通路相关分子IκB-α升高(P<0.05),p-NF-κBp65表达降低(P<0.05),肝脏病理损伤减轻,细胞凋亡减少。结论山奈酚干预通过抑制炎症反应对D-Ga IN糖/LPS诱导的小鼠AHF发挥保护作用。
Objective To investigate the effects of kaempferol on acute hepatic failure (AHF) induced by D-galactosamine (L-Ga IN) and lipopolysaccharide (LPS) in mice. Methods 37 C57BL / 6 mice were randomly divided into normal control group (n = 10), AHF model group (n = 13) and kaempferol intervention group (n = 14). AHF model mice were injected intraperitoneally with D-Ga IN (700 mg / kg) / LPS (10μg / kg) for 6 hours to establish AHF model; mice in kaempferol intervention group were injected with 5 mg / kg of kaempferol, intraperitoneal injection of D-Ga IN (700 mg / kg) / LPS (10μg / kg) for 6 h, AHF model was established. The normal control group was injected intraperitoneally with normal saline. The levels of serum ALT and AST were detected and the pathological changes of liver were observed. The expressions of TNF-α, IL-1β and IL-6 mRNA in liver tissues were detected to detect the expression of NF-κB pathway-related molecules and hepatocyte apoptosis. Results Compared with AHF model group, the kaempferol intervention group mice survival rate increased (P <0.05). Compared with the normal control group, the levels of serum ALT and AST were increased (P <0.05), the expression of inflammatory cytokines TNF-α, IL-1β and IL-6 mRNA were increased in AHF model group (P <0.05), the expression of p-NF-κBp65 was increased (P <0.05), the pathological damage of liver was serious and the apoptosis of cells was increased. Compared with AHF model group, the kaempferol intervention group The levels of serum ALT and AST were decreased (P <0.05), the expressions of inflammatory cytokines TNF-α, IL-1β and IL-6 mRNA were decreased (P <0.05) and the expression of NFκB signaling pathway- P <0.05), the expression of p-NF-κBp65 was decreased (P <0.05), the pathological damage of liver was alleviated, and the apoptosis was decreased. Conclusion The kaempferol intervention can protect the AHF induced by D-Ga IN glucose / LPS in mice by inhibiting the inflammatory response.