Effect of CaSR on activity and apoptosis of cardiomyocytes after hydrogen peroxide
Yan Shilin
Luo Yongbai
Zhu Haofeng
Xu Chao
Abstract：Objective To investigate the effect of calcium sensing receptor (CaSR) on the activity and apoptosis of cardiomyocytes after hydrogen peroxide. Methods H9C2 treated with hydrogen peroxide was recorded as model group, after treated with CaSR inhibitors (NPS2300), the H9C2 treated with hydrogen peroxide was recorded as inhibitor group, and the normal cultured H9C2 was used as the control group. The levels of CaSR in cells were detected by fluorescent quantitative PCR. Cell proliferation was measured by MTT assay. Apoptosis was measured by flow cytometry. Two 4-dinitrophenylhydrazine colorimetry assays were used to measure the lactate dehydrogenase (LDH) level in the supernatant. The level of malondialdehyde (MDA) was measured by thiobarbituric acid method. The level of superoxide dismutase (SOD) was measured by xanthine oxidase method. The levels of cleaved Caspase-3, STAT3 and p-STAT3 were measured by Western blot. Results The level of CaSR in the model group was significantly higher than that in the control group (P<0.05). The levels of CaSR in the inhibitor group were significantly lower than that in the model group (P<0.05). The rate of apoptosis, the content of MDA in the cell, the level of LDH in the supernatant of culture fluid and the level of Cleaved Caspase-3 in the cells of the model group were significantly higher than those in the control group (P<0.05). However, the rate of apoptosis, the content of MDA in the cell, the level of LDH in the supernatant of culture medium and the level of cleaved Caspase-3 in the cell were significantly lower than those in the model group (P<0.05). The cell proliferation activity, the level of SOD in cells and the level of p-STAT3 in the cells of the model group were significantly lower than those in the control group (P<0.05). The cell proliferation activity, the level of SOD in the cell and the level of p-STAT3 in the cells of the inhibitor group were significantly higher than those in the model group (P<0.05). Conclusion Inhibition of CaSR can attenuate the apoptosis of cardiomyocytes induced by hydrogen peroxide, increased cell proliferation activity, reduce oxidative damage, the mechanism of action may be related to the STAT3 signaling pathway.
Keywords：CardiomyocytesApoptosisHydrogen peroxideCaSR
Publication Date：2018-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 488-492 )