Department of Emergency (Xiangjiang Hospital), The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China.
Department of Orthopaedics, Weifang City Hanting People's Hospital, Weifang 261100, China.
Biomed Res Int. 2021 May 27;2021:5520051. doi: 10.1155/2021/5520051. eCollection 2021.
The aim of this study was to investigate the effect of cardiac troponin I-interacting kinase () on sepsis-induced myocardial dysfunction (SIMD) and further explore the underlying molecular mechanisms. In this study, a lipopolysaccharide- (LPS-) induced myocardial injury model was used. qRT-PCR was performed to detect the mRNA expression of . Western blot was conducted to quantitatively detect the expression of and apoptosis-related proteins (Bcl-2, Bax, and caspase-3). ELISA was performed to detect the content of lactate dehydrogenase (LDH) and creatine kinase (CK). TUNEL assay was used to detect the apoptosis of H9C2 cells. In LPS-induced H9C2 cells, was up regulated. Besides, the CK activity, the content of LDH, and the apoptosis of H9C2 cells were significantly increased after treatment with LPS. Silencing TNNI3K decreased the LDH release activity and CK activity and inhibited apoptosis of H9C2 cell. Further research illustrated that si-TNNI3K promoted the protein expression of Bcl-2 and decreased the protein expression of Bax and cleaved caspase-3. The study concluded that TNNI3K was upregulated in LPS-induced H9C2 cells. Importantly, functional research findings indicated that silencing TNNI3K alleviated LPS-induced H9C2 cell injury by regulating apoptosis-related proteins.
本研究旨在探讨心肌肌钙蛋白 I 相互作用激酶（）对脓毒症诱导的心肌功能障碍（SIMD）的影响，并进一步探讨其潜在的分子机制。在这项研究中，建立了脂多糖（LPS）诱导的心肌损伤模型。采用 qRT-PCR 检测心肌肌钙蛋白 I 相互作用激酶 mRNA 的表达。采用 Western blot 定量检测心肌肌钙蛋白 I 相互作用激酶和凋亡相关蛋白（Bcl-2、Bax 和 caspase-3）的表达。采用 ELISA 检测乳酸脱氢酶（LDH）和肌酸激酶（CK）的含量。采用 TUNEL 法检测 H9C2 细胞的凋亡情况。在 LPS 诱导的 H9C2 细胞中，心肌肌钙蛋白 I 相互作用激酶上调。此外，LPS 处理后 H9C2 细胞的 CK 活性、LDH 含量和细胞凋亡明显增加。沉默 TNNI3K 降低了 LDH 释放活性和 CK 活性，并抑制了 H9C2 细胞的凋亡。进一步研究表明，si-TNNI3K 促进了 Bcl-2 蛋白的表达，降低了 Bax 和 cleaved caspase-3 蛋白的表达。本研究得出结论，在 LPS 诱导的 H9C2 细胞中，心肌肌钙蛋白 I 相互作用激酶上调。重要的是，功能研究结果表明，沉默 TNNI3K 通过调节凋亡相关蛋白减轻 LPS 诱导的 H9C2 细胞损伤。
