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

It has previously been demonstrated that hyperglycemia‑induced oxidative stress and inflammation are closely associated with the development of diabetic complications, including diabetic neuropathy. Additionally, mitochondrial ATP‑sensitive potassium (Mito‑K‑ATP) channels play a homeostatic role on blood glucose regulation in organisms. Molecular hydrogen (H2) exhibits anti‑inflammatory, anti‑antioxidative and anti‑apoptotic properties and can be used to treat more than 71 diseases safely. In addition, the diabetes animal models which are set up using streptozotocin (STZ) injection, is a type of high long‑term stability, low animal mortality rate and security method. The aim of the current study was to assess the value of hydrogen‑rich saline (HS) in diabetic peripheral neuropathy (DPN) treatment and to determine its associated mechanisms in STZ‑induced diabetic experimental rats. Additionally, the effects of the Mito‑K‑ATP channels, oxidative stress, inflammatory cytokines and apoptosis on DPN were also evaluated. From week 5 of STZ injections, HS (2.5, 5 and 10 ml/kg) was injected into the rat abdominal cavity every day for a period of 4 weeks. The results of the current study demonstrated that HS significantly reduced behavioral, biochemical and molecular effects caused by DPN. However, 5‑hydroxydecanoate, a selective Mito‑K‑ATP channels general pathway inhibitor, partially eliminated the therapeutic effect of HS on DPN. These results indicated that the use of HS may be a novel strategy to treat DPN by activating the Mito‑K‑ATP pathway and reducing oxidative stress, inflammatory cytokines and apoptosis.