本文選題：慢加急性肝衰竭 + 截斷逆挽方��； 參考：《首都醫(yī)科大學學報》2017年02期

【摘要】：目的觀察截斷逆挽方對慢加急性肝衰竭(acute-on-chronic liver failure,ACLF)大鼠血清腫瘤壞死因子-α(tumor necrosis factor-α,TNF-α)含量、肝組織磷酸化c-Jun氨基末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK)及轉(zhuǎn)錄因子cJun表達的影響,探討該方干預(yù)ACLF大鼠的部分作用機制。方法選擇SPF級Wistar雄性大鼠70只,采用數(shù)字表法隨機分為正常對照組、模型組、截斷逆挽方組和JNK抑制劑SP600125(anthrapyrazolone)組,予豬血清免疫誘導大鼠形成肝纖維化模型,再聯(lián)合D-氨基半乳糖/脂多糖(D-galactosamine/lipopolysaccharide,D-Gal N/LPS)急性攻擊,建立ACLF大鼠模型。截斷逆挽方組在急性攻擊前給予截斷逆挽方連續(xù)灌胃3 d,SP600125組在急性攻擊前0.5 h腹腔注射SP600125。各組大鼠分別在急性攻擊后4、8、12 h取材。采用酶聯(lián)免疫吸附法(enzyme-linked immune sorbent assay,ELISA)檢測血清TNF-α含量,蛋白印跡法(Western blotting,WB)檢測c-Jun蛋白表達量,免疫組織化學法檢測肝組織中p-JNK蛋白表達量,HE染色觀察肝臟結(jié)構(gòu)病理變化。結(jié)果與正常組相比,模型組各時間點血清TNF-α濃度均升高,差異具有統(tǒng)計學意義(P0.01);與對應(yīng)時間點模型組相比,截斷逆挽方組及SP600125組4、8 h血清TNF-α含量明顯降低(P0.01),12 h有所升高;與正常組相比,模型組各時間點c-Jun、p-JNK表達量升高(P0.01);與模型組相比,截斷逆挽方組、SP600125組在4 h及8 h c-Jun、p-JNK表達減少(P0.05),12 h表達增多。截斷逆挽方組及SP600125組兩兩比較差異無統(tǒng)計學意義(P0.05)。結(jié)論截斷逆挽方在一定程度上可以減輕ACLF大鼠肝細胞的損傷,其作用機制可能是通過影響JNK信號通路介導的細胞凋亡,從而保護肝細胞,抑制肝衰竭。
[Abstract]:Objective To observe the effect of the truncated reverse arm on the content of serum tumor necrosis factor - alpha (tumor necrosis factor- alpha, TNF- a) in the serum of acute-on-chronic liver failure (ACLF) rats and the expression of the phosphorylated c-Jun amino terminal kinase (phosphorylated c-Jun N-terminal) and the transcription factor of the liver tissue. The partial action mechanism of pre ACLF rats was selected. Methods 70 male rats with SPF grade Wistar were selected and randomly divided into normal control group, model group, truncated reverse arm group and JNK inhibitor SP600125 (anthrapyrazolone) group. The liver fibroization model was formed in pig serum immunized rats, and then D- amino galactose / lipopolysaccharide (D-galactosa) was combined with D-. Mine/lipopolysaccharide, D-Gal N/LPS) acute attack, establish a rat model of ACLF. Truncated the reverse arm group before the acute attack of 3 D, and group SP600125 in group SP600125 before the acute attack, the rats in each group were injected with the 4,8,12 h after the acute attack. The enzyme linked immunosorbent assay (enzyme-linked immune) was used. Sorbent assay, ELISA) was used to detect the content of TNF- alpha in serum. The expression of c-Jun protein was detected by Western blot (Western blotting, WB). The expression of p-JNK protein in liver tissues was detected by immunohistochemistry. The pathological changes of liver were observed by HE staining. Compared with the normal group, the concentration of TNF- alpha in all time points of the model group increased. Study significance (P0.01); compared with the corresponding time point model group, the content of serum TNF- alpha in the truncated reverse arm group and the SP600125 group 4,8 h decreased significantly (P0.01), and the 12 h increased. Compared with the normal group, the p-JNK expression of the model group increased (P0.01) at each time point c-Jun, and the reverse arm group was truncated, and the SP600125 group was expressed in the 4 h and 8 expressions. Decreased (P0.05), 12 h expression increased. There was no significant difference between the truncated reverse arm group and the SP600125 group 22 (P0.05). Conclusion a truncated reverse arm can reduce the damage of liver cells in ACLF rats to a certain extent. The mechanism may be to protect the hepatocytes and inhibit the liver failure through the apoptosis induced by the JNK signaling pathway.

【作者單位】： 首都醫(yī)科大學中醫(yī)藥學院中醫(yī)絡(luò)病研究北京市重點實驗室;首都醫(yī)科大學附屬北京佑安醫(yī)院人工肝中心;
【基金】：首都中醫(yī)藥研究專項(14ZY01)~~
【分類號】：R285.5;R-332

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