Loganin attenuates the inflammation, oxidative stress, and apoptosis through the JAK2/STAT3 pathway in cerebral ischemia-reperfusion injury.

Loganin, a monoterpene iridoid glycoside derived from Cornus officinalis Sieb. Et Zucc, has been reported to have anti-inflammatory and antioxidant activity. Nevertheless, the potential role and molecular mechanism of loganin in cerebral ischemia-reperfusion (I/R) injury are not well-understood. The purpose of the study was to explore the functional role of loganin in the inflammation, oxidative stress, and apoptosis in cerebral I/R injury in rats MATERIALS AND METHODS: Following middle cerebral artery occlusion (MCAO), 80 mg/kg of loganin was intragastrically administered for 7 consecutive days. Neuromotor function scores were performed 24 h after the last administration, and the cerebral infarction volume was determined by TTC straining. The expressions of IL-6, IL-1β, and TNF-α in the brain tissues of MCAO rats were detected by ELISA assay. The activities of ROS, SOD, and MDA were measured by ELISA assay as well. Cell apoptosis were was tested by TUNEL straining. Western blot assay was applied for measuring the protein levels RESULTS: We observed that the expressions of IL-6, IL-1β, and TNF-α were amplitude markedly elevated in the rats following MCAO. Treatment with loganin obviously reduced these expressions in the brain tissues of MCAO rats. ELISA assay showed that ROS generation and MDA activity were increased in MCAO group and it was decreased after treatment with loganin. However, loganin increased the SOD activity, which was reduced by MCAO operation. Moreover, loganin promoted neurological function improvement and inhibited cell apoptosis in the rats after MCAO. Mechanically, loganin triggered JAK2/STAT3 phosphorylation in the rats following MCAO, and activation of JAK2/STAT3 pathway rescued the inhibition effects of loganin on the inflammation, oxidative stress, and apoptosis CONCLUSIONS: These results provide evidence that loganin may alleviate the inflammation, oxidative stress, and apoptosis through the JAK2/STAT3 pathway in MCAO rats.