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右泛醇减轻脓毒症小鼠肾和肝组织的炎症损伤及细胞凋亡。

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice.

作者信息

Zhao Xi, Zhang Siquan, Shao Hongyi

机构信息

Intensive Care Unit, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, China.

Department of Emergency Intensive Care Medicine, The Central Hospital Affiliated to Shaoxing University, Shaoxing, China.

出版信息

Bioengineered. 2022 May;13(5):11625-11635. doi: 10.1080/21655979.2022.2070585.

DOI:10.1080/21655979.2022.2070585
PMID:35510377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275904/
Abstract

Sepsis is capable of causing systemic infections resulting in multiple organ damage. Dexpanthenol (DXP) has been reported to protect against kidney and liver injury. Therefore, this paper attempts to explore the role of DXP in sepsis-induced kidney and liver injury. A mice model of sepsis was established using the cecal ligation and puncture (CLP) method. The expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein (MCP)-1 in the serum of mice were measured utilizing enzyme linked immunosorbent assay (ELISA). Additionally, the damage of kidney and liver tissues in CLP-induced mice was determined by their respective commercial kits, western blot, and hematoxylin-eosin (HE) staining kits. The apoptosis of kidney and liver tissues in CLP-induced mice was assessed by means of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot. It was observed that DXP decreased the expressions of TNF-α, IL-1β, IL-6, and MCP-1 in the serum of CLP-induced mice, attenuated the functional impairment, pathological damage, inflammation, and cell apoptosis of kidney tissue. Meanwhile, DXP decreased the functional impairment of liver in CLP-induced mice, reduced the levels of inflammatory factors and antioxidant enzymes, attenuated liver pathological damage, and decreased cell apoptosis in liver tissues. In conclusion, DXP attenuates inflammatory damage and apoptosis in kidney and liver organs in a sepsis model.

摘要

脓毒症能够引发全身感染,导致多器官损伤。据报道,泛醇(DXP)可预防肾脏和肝脏损伤。因此,本文旨在探讨DXP在脓毒症诱导的肾脏和肝脏损伤中的作用。采用盲肠结扎和穿刺(CLP)方法建立脓毒症小鼠模型。利用酶联免疫吸附测定(ELISA)检测小鼠血清中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6和单核细胞趋化蛋白(MCP)-1的表达。此外,通过各自的商业试剂盒、蛋白质印迹法和苏木精-伊红(HE)染色试剂盒测定CLP诱导小鼠的肾脏和肝脏组织损伤。通过末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)和蛋白质印迹法评估CLP诱导小鼠肾脏和肝脏组织的凋亡。观察到DXP降低了CLP诱导小鼠血清中TNF-α、IL-1β、IL-6和MCP-1的表达,减轻了肾脏组织的功能损害、病理损伤、炎症和细胞凋亡。同时,DXP降低了CLP诱导小鼠肝脏的功能损害,降低了炎症因子和抗氧化酶水平,减轻了肝脏病理损伤,并减少了肝脏组织中的细胞凋亡。总之,在脓毒症模型中,DXP减轻了肾脏和肝脏器官的炎症损伤和凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/995138e11fd2/KBIE_A_2070585_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/561bdd9470c5/KBIE_A_2070585_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/43925fe4bce7/KBIE_A_2070585_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/6389656b6e00/KBIE_A_2070585_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/c8b83fbdd339/KBIE_A_2070585_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/dcb8a99ddb21/KBIE_A_2070585_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/995138e11fd2/KBIE_A_2070585_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/561bdd9470c5/KBIE_A_2070585_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/43925fe4bce7/KBIE_A_2070585_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/6389656b6e00/KBIE_A_2070585_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/c8b83fbdd339/KBIE_A_2070585_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/dcb8a99ddb21/KBIE_A_2070585_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b540/9275904/995138e11fd2/KBIE_A_2070585_F0005_OC.jpg

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