[1]曹 春,何凯明,陈 伟,等.富辛酸肠内营养通过抑制JNK诱导的肝细胞凋亡缓解脓毒症急 性肝损伤[J].肠外与肠内营养杂志,2021,(05):262-266.[doi:10.16151/j.1007-810x.2021.05.002]
 CAO Chun,HE Kai-ming,CHEN Wei,et al.Octanoic acid-rich enteral nutrition could alleviate sepsis-induced acute liver injury through inhibition of JNK-mediated hepatocyte apoptosis[J].PARENTERAL & ENTERAL NUTRITION,2021,(05):262-266.[doi:10.16151/j.1007-810x.2021.05.002]
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富辛酸肠内营养通过抑制JNK诱导的肝细胞凋亡缓解脓毒症急 性肝损伤
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《肠外与肠内营养》杂志[ISSN:1007-810X/CN:32-1477/R]

卷:
期数:
2021年05期
页码:
262-266
栏目:
论著
出版日期:
2021-09-10

文章信息/Info

Title:
Octanoic acid-rich enteral nutrition could alleviate sepsis-induced acute liver injury through inhibition of JNK-mediated hepatocyte apoptosis
作者:
曹 春何凯明陈 伟杜 鹏
苏州大学附属第二医院普通外科,江苏苏州 215000
Author(s):
CAO Chun HE Kai-ming CHEN Wei DU Peng
Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou 215000, Jiangsu, China
关键词:
富辛酸肠内营养 脓毒症 急性肝损伤 JNK 凋亡
Keywords:
Octanoic acid-rich enteral nutrition Sepsis Acute liver injury JNK Apoptosis
分类号:
R459.7,R459.3
DOI:
10.16151/j.1007-810x.2021.05.002
文献标志码:
A
摘要:
目的:探讨富辛酸肠内营养对脓毒症急性肝损伤的保护作用及可能机制。 方法:首先,将 24只 SD 大鼠随机分为四组:对照组、脓毒症组、脓毒症+肠内营养组、脓毒症+肠内营养+辛酸组,腹腔内注射脂多糖(LPS,5mg/kg)建立内毒血症模型后分别给予 3 d 肠内营养[100 kcal/(kg·d)]或富辛酸肠内营养[辛酸 0.5 g/kg,总能量 100 kcal/(kg·d)]。肝脏 HE 染色,生化分析仪检测血清 ALT、AST 和 LDH 水平,ELISA 检测血清及肝脏 IL-6、IL-1β 和TNF-α水平,Western blotting检测凋亡相关蛋白 Bax、Bcl及 Cleaved Caspase-3的表达水平及 JNK的活性。其次,将30 只 SD 大鼠随机分为五组:对照组、脓毒症组、脓毒症+肠内营养+辛酸组、脓毒症+肠内营养+辛酸+anisomycin(JNK激活剂)组、脓毒症+SP600125(JNK抑制剂)组。各组腹腔内注射相应的药物并予以相应的营养支持,余处理及检测方法同前。 结果:与脓毒症+肠内营养组相比,脓毒症+肠内营养+辛酸组肝脏病理损伤明显好转,肝酶ALT、AST及 LDH水平明显下降,肝脏及血清中炎症因子 IL-6、IL-1β 和 TNF-α 水平明显下降;下调肝脏中 Bax和Cleaved Caspase-3 蛋白表达,上调 Bcl 蛋白表达,抑制 JNK 的活性。anisomycin 显著减弱富辛酸肠内营养对肝脏JNK抑制和抗凋亡的作用及其对脓毒症急性肝损伤的保护作用。SP600125能够显著抑制肝脏 JNK活性和凋亡,显示出与富辛酸肠内营养相同的保护脓毒症急性肝损伤的作用。 结论:富辛酸肠内营养通过抑制 JNK诱导的肝细胞凋亡保护脓毒症急性肝损伤。
Abstract:
Objective: To explore the protective effect of octanoic acid (OA)-rich enteral nutrition (EN) on acute liver injury (ALI) induced by sepsis and the underlying mechanisms. Methods: Twenty-four rats were randomly divided into four groups: sham, lipopolysaccharides (LPS), LPS + EN and LPS + EN + OA groups. In three groups (LPS, LPS + EN and LPS + EN + OA), rats were intraperitoneally injected with LPS (5 mg/kg) to induce endotoxemia. EN and OA-rich EN were then administered in the latter two groups via gastric tube for 3 days, respectively. Liver histopathology, serum liver enzymes, inflammatory cytokines of serum and liver, the expression of liver apoptosis-related protein and JNK activity were measured. Subsequently, another experiment containing five groups [Sham, LPS, LPS + EN + OA, LPS + EN + OA + anisomycin (AN) and LPS + SP600125 (SP)] (six rats per group) was carried out to evaluate the involvement of JNK in the protective effects of OA-rich EN in sepsis. Results: Compared with the LPS + EN group, OA-rich EN decreased histopathological scores of liver, the levels of liver enzymes and the inflammatory cytokines of serum and liver. OA-rich EN also decreased the expression of Bax and cleaved caspase-3, increased the expression of Bcl and inhibited JNK activity in liver. The protective effect of inhibition of JNK activity and hepatocyte apoptosis conferred by OA-rich EN on ALI was aggravated by AN. Moreover, inhibition of JNK activity conferred by SP inhibited apoptosis and showed the similar effect on ALI compared with the LPS + EN + OA group. Conclusions: OArich EN could alleviate ALI via inhibiting JNK-induced hepatocyte apoptosis during sepsis.

参考文献/References:


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备注/Memo

备注/Memo:
基金项目 :苏州市科技局项目(SYS2019069);北京清华长庚医院董家鸿院士肝胆胰外科团队(SZYJTD201803) 作者简介 :曹 春,主治医师,医学博士,从事普通外科。E-mail:caochunnj@163.com 通讯作者 :杜 鹏,E-mail:dupeng3331@163.com
更新日期/Last Update: 1900-01-01