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目的:探讨不同剂量丁酸钠预处理对内毒素性肝损伤小鼠促炎与抗炎因子的影响。方法:取健康雄性昆明小鼠72只,随机分为6组(n=12):正常组、模型组、联苯双酯组、丁酸钠低、中和高剂量组。应用脂多糖10mg/kg腹腔注射小鼠诱导内毒素肝损伤模型。造模后6h,检测小鼠血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平,酶联免疫吸附试验(ELISA)检测小鼠血清肿瘤坏死因子(TNF-α)、干扰素(IFN-γ)、白介素-4(IL-4)和IL-10的含量。结果:与模型组相比,丁酸钠低、中和高剂量组血清ALT、AST、TNF-α和IFN-γ含量明显降低(P<0.05),IL-4和IL-10量明显增高(P<0.05)。但丁酸钠各剂量组之间差异无统计学意义。结论:丁酸钠预处理可以抑制内毒素肝损伤小鼠炎症反应,其机制可能与抑制TNF-α和IFN-γ的释放,提高IL-4和IL-10的含量,促进致炎介质与抗炎介质的平衡有关。
Objective: To investigate the effects of different doses of sodium butyrate on proinflammatory and anti-inflammatory cytokines in endotoxic liver injury mice. Methods: Seventy two healthy male Kunming mice were randomly divided into 6 groups (n = 12): normal group, model group, bifendate group, sodium butyrate low, medium and high dose groups. Lipopolysaccharide 10mg / kg intraperitoneal injection of endotoxin induced liver injury model in mice. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured 6 h after model establishment. Serum tumor necrosis factor (TNF-α) was measured by enzyme linked immunosorbent assay (ELISA) ), Interferon (IFN-γ), interleukin-4 (IL-4) and IL-10. Results: Compared with model group, serum ALT, AST, TNF-αand IFN-γlevels in low, middle and high doses of sodium butyrate significantly decreased (P <0.05) and IL-4 and IL- P <0.05). However, there was no significant difference between each dosage group of sodium butyrate. CONCLUSION: Pretreatment with sodium butyrate can inhibit the inflammatory response in LPS-induced liver injury in mice. The mechanism may be that it inhibits the release of TNF-α and IFN-γ, increases the content of IL-4 and IL-10, Inflammatory media balance.