[Inhibition of gap junctional intercellular communication protects astrocytes from hypoxia/reoxygenation injury]

To investigate the effects of inhibiting gap junctional intercellular communication on hypoxia/reoxygenation injury in astrocytes.

Primary cultured cerebral cortical astrocytes of neonate rats were divided into normal control group, hypoxia reoxygenation injury group and 18-α-glycyrrhetinic acid and oleamide (gap junctional intercellular channel inhibitors) group. The gap junction intercellular communication was determined by Parachute assay. The viability of astrocyes was detected by MTT assay. The apoptosis of astrocytes were detected with annexin V/PI and Hoechst 33258 staining.

Compared with the normal control group, the gap junctional function of astrocytes was increased significantly in ischemia/reperfusion group (P<0.01), the surviving fraction of astrocytes decreased significantly (P<0.01) and its cell apoptosis ratio increased significantly (P<0.01). Compared with the ischemia/reperfusion group, the gap junctional function of astrocytes in18-α-glycyrrhetinic acid and oleamide group decreased significantly (P<0.01), the viability of astrocytes increased significantly (P<0.01), while cell apoptosis decreased significantly (P<0.01).

Inhibition of intercellular gap junction has protective effect against hypoxia/reoxygenation injury in astrocytes.