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Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2017 Nov 28;42(11):1263-1269. doi: 10.11817/j.issn.1672-7347.2017.11.004.

[Cordyceps sinensis protects HK2 cells from ischemia-reperfusion injury through Sirt1 pathway].

[Article in Chinese; Abstract available in Chinese from the publisher]

Author information

1
Department of Nephrology, Xiangya Hospital, Central South University, Changsha 410008; Department of Nephrology, Third Hospital of Changsha, Changsha 410015, China.
2
Department of Nephrology, Xiangya Hospital, Central South University, Changsha 410008, China.
3
Department of Respiratory Medicine, First Hospital of Changsha, Changsha 410005, China.
4
Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha 410008, China.
5
Department of Nephrology, Third Hospital of Changsha, Changsha 410015, China.

Abstract

in English, Chinese

To investigate the effects of Cordyceps sinensis (CS) on cellular apoptosis and Sirt1 expression in HK2 cells followed by ischemia-reperfusion (I/R).
 Methods: HK2 cells were incubated with different concentrations of CS (10, 20, 40, 80, 160, 320 mg/L) for 24 hours, and the optimal concentration of CS was selected by measuring cell proliferation. The confluent HK2 cells were incubated with 0.01 μmol/L antimycin A for 2 hours to induce ischemia in vitro, and then the reperfusion was achieved by incubating cells with glucose-replete complete growth medium for 24 hours. HK2 cells were divided into 4 groups: a control group, an I/R group, an I/R+CS (160 mg/L) group, and an I/R+CS (160 mg/L)+Sirtinol (25 μmol/L) group. Twenty-four hours later, total RNA and protein were collected. The cell proliferation was evaluated by MTT assay; the mRNA and protein expression of Sirt1 and the cleaved caspase-3 were measured by qRT-PCR and Western blot, respectively. The cellular apoptosis rate was determined by Annexin V-FITC/PI double staining and flow cytometry.
 Results: Certain concentrations (10-160 mg/L) of CS did not show effect on the proliferation of HK2 cells (P>0.05), while 320 mg/L of CS inhibited cell proliferation significantly (P<0.01); compared with the control group, the mRNA and protein expressions of Sirt1 and the cleaved caspase-3 in the I/R group were up-regulated (P<0.01) and the apoptosis rate was extremely high; compared with the I/R group, CS significantly up-regulated Sirt1 mRNA and protein expression (P<0.01) while down-regulated cleaved caspase-3 mRNA and protein levels (P<0.01), and reduced apoptosis rate (P<0.05). The effects of CS were blocked in the presence of sirtinol, an inhibitor of CS.
 Conclusion: CS protects HK2 cells from I/R injury through activation of Sirt1 pathway.

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