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丹参酮IIA磺酸钠减轻脂多糖诱导的小鼠肠道损伤。

Tanshinone IIA Sodium Sulfonate Attenuates LPS-Induced Intestinal Injury in Mice.

作者信息

Yang Xin-Jing, Qian Jin-Xian, Wei Yao, Guo Qiang, Jin Jun, Sun Xue, Liu Sheng-Lan, Xu Chun-Fang, Zhang Guo-Xing

机构信息

Department of Intensive Care Unit, The First Affiliated Hospital, Soochow University, 188 Shi-Zi Road, Suzhou 215006, China.

Department of Emergency, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, China.

出版信息

Gastroenterol Res Pract. 2018 Mar 8;2018:9867150. doi: 10.1155/2018/9867150. eCollection 2018.

Abstract

BACKGROUND

Tanshinone IIA sodium sulfonate (TSS) is known to possess anti-inflammatory effects and has exhibited protective effects in various inflammatory conditions; however, its role in lipopolysaccharide- (LPS-) induced intestinal injury is still unknown.

OBJECTIVE

The present study is designed to explore the role and possible mechanism of TSS in LPS-induced intestinal injury.

METHODS

Male C57BL/6J mice, challenged with intraperitoneal LPS injection, were treated with or without TSS 0.5 h prior to LPS exposure. At 1, 6, and 12 h after LPS injection, mice were sacrificed, and the small intestine was excised. The intestinal tissue injury was analyzed by HE staining. Inflammatory factors (TNF-, IL-1, and IL-6) in the intestinal tissue were examined by ELISA and RT-PCR. In addition, expressions of autophagy markers (microtubule-associated light chain 3 (LC3) and Beclin-1) were detected by western blot and RT-PCR. A number of autophagosomes were also observed under electron microscopy.

RESULTS

TSS treatment significantly attenuated small intestinal epithelium injury induced by LPS. LPS-induced release of inflammatory mediators, including TNF-, IL-1, and IL-6, were markedly inhibited by TSS. Furthermore, TSS treatment could effectively upregulate LPS-induced decrease of autophagy levels, as evidenced by the increased expression of LC3 and Beclin-1, and more autophagosomes.

CONCLUSION

The protective effect of TSS on LPS-induced small intestinal injury may be attributed to the inhibition of inflammatory factors and promotion of autophagy levels. The present study may provide novel insight into the molecular mechanisms of TSS on the treatment of intestinal injury.

摘要

背景

丹参酮IIA磺酸钠(TSS)具有抗炎作用,已在多种炎症条件下表现出保护作用;然而,其在脂多糖(LPS)诱导的肠道损伤中的作用仍不清楚。

目的

本研究旨在探讨TSS在LPS诱导的肠道损伤中的作用及可能机制。

方法

雄性C57BL/6J小鼠腹腔注射LPS进行攻击,在LPS暴露前0.5小时给予或不给予TSS治疗。LPS注射后1、6和12小时,处死小鼠并切除小肠。通过苏木精-伊红(HE)染色分析肠道组织损伤。采用酶联免疫吸附测定(ELISA)和逆转录-聚合酶链反应(RT-PCR)检测肠道组织中的炎症因子(肿瘤坏死因子-α、白细胞介素-1和白细胞介素-6)。此外,通过蛋白质免疫印迹法(western blot)和RT-PCR检测自噬标志物(微管相关轻链3(LC3)和Beclin-1)的表达。在电子显微镜下也观察到了大量自噬体。

结果

TSS治疗显著减轻了LPS诱导的小肠上皮损伤。TSS显著抑制了LPS诱导的包括肿瘤坏死因子-α、白细胞介素-1和白细胞介素-6在内的炎症介质释放。此外,TSS治疗可有效上调LPS诱导的自噬水平降低,这通过LC3和Beclin-1表达增加以及更多自噬体得以证明。

结论

TSS对LPS诱导的小肠损伤的保护作用可能归因于对炎症因子的抑制和自噬水平的促进。本研究可能为TSS治疗肠道损伤的分子机制提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/5863351/823477c0b63c/GRP2018-9867150.001.jpg

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