雷公藤红素对高糖诱导的H9C2细胞损伤的保护作用

doi:10.3969/j.issn.2095-9400.2020.01.005

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Abstract Objective: To simulate in vitro the cellular model of DCM by high glucose culture medium of rat cardiomyocytes H9C2 and to study the protective effect and mechanism of Celastrol on H9C2 cells. Methods: In the experiment, low glucose group (5.6 mmol/L), isoosmotic group (mannitol isoosmotic culture), high glucose treatment group (30 mmol/L) and Celastrol group (high glucose culture and intervention with 10 ng/mL and 100 ng/mL Celastrol) were established. MTT assays were used to analyze the viability of H9C2 cells in high glucose treatment group and Celastrol group. Reactive oxygen species cluster fluorescence probe staining and flow cytometry were performed to analyze the production of ROS in H9C2 cells induced by high glucose culture and intervened with Celastrol. The mRNA and protein expression level of NF-κB, TGF-1β and IL-1β were detected by RT-PCR and Western blot. Results: Significant inhibitory effects on the viability of H9C2 cells were observed in high glucose treatment group, with statistically significant difference compared with the low glucose group (P<0.05). The proliferation inhibitory effect was attenuated when intervened with different concentrations of Celastrol. The ROS levels in high glucose treatment group was significantly higher than the low glucose group (P<0.05), and the ROS levels were decreased after intervention of 100 ng/mL Celastrol. RT-PCR, Western blot results showed that the mRNA and protein expression levels of NF-κB, TGF-1β and IL-1β genes were up-regulated in high glucose treatment group, compared with low glucose and the isotonic group, the differences were statistically significant (P<0.05). The mRNA and protein expression levels of NF-κB, TGF-1β and IL-1β in 10 ng/mL and 100 ng/mL Celastrol group were down-regulated compared with high glucose treatment group, the differences being significant (P<0.05). Conclusion: Celastrol could inhibit production of ROS in H9C2 cells in high glucose culture and reduce the growth inhibition effect on cells, thus producting protective effects on cardiac myocytes. The mechanism may be related to the inhibited expression of inflammatory factor-related genes.

Key words： diabetic cardiomyopathies Celastrol reactive oxygen species H9C2 cells

Received: 23 June 2019

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	WU Zhang
	LYU Wang
	CHEN Xinguo
	JIN Shuang
	CHEN Linglong
	LU Zhongqiu

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2020.01.005 OR https://xb.wmu.edu.cn/EN/Y2020/V50/I1/24

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