嗜热菌 HB27 锰超氧化物歧化酶对盐酸诱导的大鼠化学性膀胱炎的保护作用。

The protective effect of manganese superoxide dismutase from thermophilic bacterium HB27 on hydrochloric acid-induced chemical cystitis in rats.

机构信息

Department of Urology, The Affiliated Hospital of Jiaxing University, Jiaxing, 314001, Zhejiang, China.

Department of Pharmacology, College of Medical, Jiaxing University, Jiaxing, Zhejiang, 314001, People's Republic of China.

出版信息

Int Urol Nephrol. 2022 Jul;54(7):1681-1691. doi: 10.1007/s11255-021-03054-8. Epub 2021 Nov 16.

DOI:10.1007/s11255-021-03054-8

PMID:34783980

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9184365/

Abstract

PURPOSE

To evaluate the effects of manganese superoxide dismutase (Mn-SOD) from thermophilic bacterium HB27 (name as Tt-SOD) on chemical cystitis.

METHODS

Control and experimental rats were infused by intravesical saline or hydrochloric acid (HCl) on the first day of the experiments. Saline, sodium hyaluronate (SH) or Tt-SOD were infused intravesically once a day for three consequent days. On the fifth day, the rats were weighted and sacrificed following a pain threshold test. The bladder was harvested for histological and biochemical analyses.

RESULTS

Tt-SOD could reduce the bladder index, infiltration of inflammatory cells in tissues, serum inflammatory factors and SOD levels, mRNA expression of inflammatory factors in tissues, and increase perineal mechanical pain threshold and serum MDA and ROS levels in HCl-induced chemical cystitis. Furthermore, Tt-SOD alleviated inflammation and oxidative stress by the negative regulation of the NF-κB p65 and p38 MAPK signaling pathway.

CONCLUSIONS

Intravesical instillation of Tt-SOD provides protective effects against HCl-induced cystitis.

摘要

目的

评估嗜热菌 HB27 来源的锰超氧化物歧化酶（Mn-SOD，命名为 Tt-SOD）对化学性膀胱炎的作用。

方法

实验第一天，对照组和实验组大鼠通过膀胱内灌注生理盐水或盐酸（HCl）。连续 3 天，每天一次膀胱内灌注生理盐水、透明质酸钠（SH）或 Tt-SOD。第 5 天，进行疼痛阈值测试后称重并处死大鼠。采集膀胱组织进行组织学和生化分析。

结果

Tt-SOD 可降低膀胱指数、组织浸润的炎性细胞、血清炎性因子和 SOD 水平、组织中炎性因子的 mRNA 表达，增加盐酸诱导的化学性膀胱炎大鼠的会阴部机械痛阈值以及血清 MDA 和 ROS 水平。此外，Tt-SOD 通过负向调控 NF-κB p65 和 p38 MAPK 信号通路缓解炎症和氧化应激。