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肠淋巴管结扎对重症急性胰腺炎大鼠肺损伤的影响。

Influence of Intestinal Lymphatic Ligation on Pulmonary Injury in Rats with Severe Acute Pancreatitis.

机构信息

Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, 646000, China.

Chengdu Vocational and Technical College, Chengdu, 610000, China.

出版信息

Curr Med Sci. 2022 Aug;42(4):711-719. doi: 10.1007/s11596-022-2594-4. Epub 2022 Aug 13.

DOI:10.1007/s11596-022-2594-4
PMID:35963948
Abstract

OBJECTIVE

The present study explored the mechanisms involved in intestinal lymphatic ligation in rats with severe acute pancreatitis (SAP).

METHODS

Male Sprague Dawley rats were randomly divided into 4 groups: saline group, saline+ligation group, SAP group, and SAP+ligation group. Rats in the SAP group were administered sodium taurocholate solution. Isolated mesenteric lymph duct ligation was administered to the saline+ligation and SAP+ligation groups. Endotoxin (ET), nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), myeloperoxidase (MPO), and superoxide dismutase (SOD) were detected. Nuclear factor-κB (NF-κB) and intercellular cell adhesion molecule-1 (ICAM-1) proteins were observed. The mRNA of inducible nitric oxide synthase(iNOS) and Toll-like receptor 4 (TLR4) was detected by PCR.

RESULTS

Pathomorphological analysis showed that necrosis was present in the lung of rats in the SAP group, but only mild lesions in the SAP+ligation group. ET, NO, TNF-α, and IL-1 in the serum and lung tissue were significantly decreased and MPO was increased in the SAP+ligation group as compared with the SAP group. However, MPO was increased. The expression of NF-κB and ICAM-1, either iNOS or TLR4, was upregulated in the SAP group, but downregulated in the SAP+ligation group. Intestinal lymph duct ligation prevented ET translocation, the release of inflammation factors, and inflammation injury.

CONCLUSION

The intestinal lymph duct ligation could alleviate SAP-induced pulmonary injury by suppressing NF-κB activation in rats.

摘要

目的

本研究旨在探讨严重急性胰腺炎(SAP)大鼠肠淋巴管结扎相关的机制。

方法

雄性 Sprague Dawley 大鼠随机分为 4 组:生理盐水组、生理盐水+结扎组、SAP 组和 SAP+结扎组。SAP 组大鼠给予牛磺胆酸钠溶液。结扎分离肠系膜淋巴管,应用于生理盐水+结扎组和 SAP+结扎组。检测内毒素(ET)、一氧化氮(NO)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、髓过氧化物酶(MPO)和超氧化物歧化酶(SOD)。观察核因子-κB(NF-κB)和细胞间黏附分子-1(ICAM-1)蛋白。通过 PCR 检测诱导型一氧化氮合酶(iNOS)和 Toll 样受体 4(TLR4)的 mRNA。

结果

形态学分析表明,SAP 组大鼠肺组织出现坏死,但 SAP+结扎组仅出现轻度病变。与 SAP 组相比,SAP+结扎组血清和肺组织中 ET、NO、TNF-α 和 IL-1 明显减少,MPO 增加。但 MPO 增加。SAP 组 NF-κB 和 ICAM-1 表达上调,iNOS 或 TLR4 表达上调,但 SAP+结扎组 NF-κB 和 ICAM-1 表达下调,iNOS 或 TLR4 表达下调。肠淋巴管结扎可防止 ET 易位、炎症因子释放和炎症损伤。

结论

在大鼠中,肠淋巴管结扎可通过抑制 NF-κB 激活来减轻 SAP 诱导的肺损伤。

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