Abstract:

Objective This study intends to verify whether the regulation of CK1δ and PER1 on ischemic stroke may be achieved by regulating the function of mitochondria. Methods In this experiment，mouse microglia （BV2 cells）were used as the research objects. The cells were treated with cobalt chloride（CoCl2）to simulate the hypoxic state of the cells during stroke.The functions of Per1 and mitochondria were detected by inhibiting，knock⁃ ing down and overexpressing CK1δ. Results The overall expression levels of CK1δ and Per1 in BV2 cells treated with 200 μmol/L CoCl2 for 24 h were decreased.Under the hypoxic conditions，the inhibited and silenced CK1δ increased PER1 protein levels in the nucleus，elevated Mfn1 expression，and suppressed Drp1 expression，but the overexpressed CK1 δ suppressed Mfn1 expression and elevated Drp1 expression. In addition，the proportion of linear mitochondria was elevated upon CK1δ inhibition or silencing，while the proportion of punctate mitochondria was significantly increased upon CK1δ overexpression. Conclusion Under hypoxic conditions，CK1δ and PER1 can regulate the mitochondrial morphology of BV2 cells so that ischemic stroke is mediated.

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