Protective effects of hydrogen‑rich saline against experimental diabetic peripheral neuropathy via activation of the mitochondrial ATP‑sensitive potassium channel channels in rats.

Abstract

Using a streptozotocin (STZ)-induced rat model of diabetic peripheral neuropathy (DPN), this study examined the effects of hydrogen-rich saline (HS) administered intraperitoneally at doses of 2.5, 5, and 10 ml/kg daily for 4 weeks beginning at week 5 post-STZ injection. HS significantly ameliorated behavioral, biochemical, and molecular markers associated with DPN, including reductions in oxidative stress, pro-inflammatory cytokines, and apoptotic activity. Co-administration of 5-hydroxydecanoate, a selective inhibitor of mitochondrial ATP-sensitive potassium (Mito-K-ATP) channels, partially reversed these beneficial effects, implicating Mito-K-ATP channel activation as a key mechanistic component. The findings suggest that HS exerts neuroprotective effects in DPN through a pathway involving Mito-K-ATP channel activation alongside suppression of oxidative and inflammatory responses.

Mechanism

Hydrogen-rich saline activates mitochondrial ATP-sensitive potassium (Mito-K-ATP) channels, which in turn suppresses hyperglycemia-induced oxidative stress, pro-inflammatory cytokine release, and apoptosis, thereby reducing peripheral nerve damage in diabetic rats.