Propofol protects against oxygen/glucose deprivation‑induced cell injury via gap junction inhibition in astrocytes.

Stroke is one of the leading causes of mortality and disability worldwide with limited clinical therapies available. The present study isolated primary astrocytes from the brains of rats and treated them with oxygen‑glucose deprivation and re‑oxygenation (OGD/R) to mimic hypoxia/reperfusion (H/R) injury in vitro to investigate stroke. It was revealed that propofol (2,6‑diisopropylphenol), an intravenous sedative and anesthetic agent, protected against oxygen/glucose‑deprivation (OGD) and induced cell injury. Furthermore, propofol exerted a protective effect by inhibiting gap junction function, which was also revealed to promote cell death in astrocytes. The present study further identified that propofol suppressed gap junction function by downregulating the protein expression levels of connexin43 (Cx43), which is one of the most essential components of gap junctions in astrocytes. In addition, when the expression levels of Cx43 were downregulated using small interfering RNA, OGD/R‑induced cell death was decreased. Conversely, cell death was enhanced when Cx43 was overexpressed, which was reversed following propofol treatment. In summary, propofol protects against OGD‑induced injury in astrocytes by decreasing the protein expression levels of Cx43 and suppressing gap junction function. The present study improved our understanding of how propofol protects astrocytes from OGD/R‑induced injury.