Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis.
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis.
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Hsp22 通过抑制炎症、氧化应激和细胞凋亡来改善脂多糖诱导的心肌损伤。
DOI：
10.1080/21655979.2021.2010315
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发表时间：
2021-12
期刊：
影响因子：
4.9
通讯作者：
Cheng XS
中科院分区：
文献类型：
--
作者：
Yu Y;Hu LL;Liu L;Yu LL;Li JP;Rao JA;Zhu LJ;Bao HH;Cheng XS
脓毒症诱导的心肌功能障碍（SIMD）在脓毒症休克患者中普遍存在，并与高发病率和死亡率相关。热休克蛋白22（Heat shock protein 22，Hsp 22）是一种小分子热休克蛋白家族，具有多种生物学功能。然而，热休克蛋白22在脂多糖（LPS）诱导的心肌损伤中的功能尚未确定。本研究旨在探讨热休克蛋白22在脂多糖诱导的心肌损伤中的作用机制。在本研究中，将雄性C57 BL/6小鼠随机分配到对照组、LPS处理组和LPS + Hsp 22处理组后，进行相关超声心动图和染色以仔细检查心脏病理学。根据酶联免疫吸附试验和蛋白质印迹试验的结果，提出了合理的机制。Hsp 22对LPS诱导的心肌损伤的保护作用出现，证明从肌酐激酶MB（CK-MB），乳酸脱氢酶（LDH）的水平降低，并增强心功能。LPS给药后引起的炎性细胞因子（IL-1β、IL-6、TNF-α和NLRP 3）的峰被Hsp 22预处理减弱。此外，超氧化物歧化酶（SOD）的活性和B细胞淋巴瘤-2（Bcl 2）的水平增加热休克蛋白22治疗导致降低LPS诱导的氧化应激和心肌细胞凋亡。总之，Hsp 22过表达通过靶向心肌细胞中的炎症、氧化应激和凋亡来抑制LPS诱导的心肌损伤，为该蛋白用于治疗SIMD铺平了道路。
Sepsis-induced myocardial dysfunction (SIMD) is ubiquitous in septic shock patients and is associated with high morbidity and mortality rates. Heat shock protein 22 (Hsp22), which belongs to the small HSP family of proteins, is involved in several biological functions. However, the function of Hsp22 in lipopolysaccharide (LPS)-induced myocardial injury is not yet established. This study was aimed at investigating the underlying mechanistic aspects of Hsp22 in myocardial injury induced by LPS. In this study, following the random assignment of male C57BL/6 mice into control, LPS-treated, and LPS + Hsp22 treated groups, relevant echocardiograms and staining were performed to scrutinize the cardiac pathology. Plausible mechanisms were proposed based on the findings of the enzyme-linked immunosorbent assay and Western blotting assay. A protective role of Hsp22 against LPS-induced myocardial injury emerged, as evidenced from decreased levels of creatinine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and enhanced cardiac function. The post-LPS administration-caused spike in inflammatory cytokines (IL-1β, IL-6, TNF-α and NLRP3) was attenuated by the Hsp22 pre-treatment. In addition, superoxide dismutase (SOD) activity and B-cell lymphoma-2 (Bcl2) levels were augmented by Hsp22 treatment resulting in lowering of LPS-induced oxidative stress and cardiomyocyte apoptosis. In summary, the suppression of LPS-induced myocardial injury by Hsp22 overexpression via targeting of inflammation, oxidative stress, and apoptosis in cardiomyocytes paves the way for this protein to be employed in the therapy of SIMD.
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影响因子：
11.4
作者：
Fan H;Ding R;Liu W;Zhang X;Li R;Wei B;Su S;Jin F;Wei C;He X;Li X;Duan C
通讯作者：
Duan C
DOI：
10.2217/nnm.15.45
发表时间：
2015
期刊：
Nanomedicine (London, England)
影响因子：
--
作者：
Prasad LK;O'Mary H;Cui Z
通讯作者：
Cui Z
影响因子：
5.6
作者：
Lan, Yin;Wang, Yi;Zeng, Qiutang
通讯作者：
Zeng, Qiutang
DOI：
10.1016/s0167-4781(01)00237-8
发表时间：
2001-07-30
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
影响因子：
--
作者：
Kappé, G;Verschuure, P;De Jong, WW
通讯作者：
De Jong, WW
DOI：
10.1161/circoutcomes.117.004040
发表时间：
2018-02-01
影响因子：
6.9
作者：
Frencken, Jos F.;Donker, Dirk W.;Cremer, Olaf L.
通讯作者：
Cremer, Olaf L.