Abstract
Hyperglycemia can be considered a determining factor in the development of diabetic neuropathy as well as neuropathic pain. There is a relationship between the excessive production of reactive oxygen species (ROS) and the pathogenesis of diabetic neuropathic pain. Taxifolin, on the other hand, is a flavonoid that has been documented to inhibit ROS production. To investigate the effects of taxifolin, which has antioxidant and neuroprotective effects, on alloxan-induced hyperglycemia-induced neuropathy and neuropathic pain, biochemically and histopathologically. The albino Wistar male rats were divided into 3 groups: healthy group (HG), only alloxan group (AXG) and alloxan+taxifolin group (ATG). Hyperglycemia in animals was caused through intraperitoneal injection of alloxan at a dose of 120 mg/kg. Paw pain thresholds of animals were measured using Basile algesimeter. Sciatic nerve tissues were examined biochemically and histopathologically in order to evaluate neuropathy. Our experimental results revealed that taxifolin significantly prevented the increase of plasma glucose concentration level with alloxan administration, the decrease of the paw pain threshold related to hyperglycemia, the change of oxidant-antioxidant balance in the sciatic nerve tissue in favor of oxidants, and the deterioration of tissue morphology in animals. Our experimental results indicate that taxifolin alleviates alloxan-induced hyperglycemia-related neuropathy and neuropathic pain.
Highlights
Hyperglycemia can be considered a determining factor in the development of diabetic neuropathy as well as neuropathic pain
Our experimental results revealed that taxifolin significantly prevented the increase of plasma glucose concentration level with alloxan administration, the decrease of the paw pain threshold related to hyperglycemia, the change of oxidant–antioxidant balance in the sciatic nerve tissue in favor of oxidants, and the deterioration of tissue morphology in animals
Our experimental results indicate that taxifolin alleviates alloxan-induced hyperglycemiarelated neuropathy and neuropathic pain
Summary
Hyperglycemia can be considered a determining factor in the development of diabetic neuropathy as well as neuropathic pain. Former studies have suggested that excessive mitochondrial glucose loading increases electron transfer to oxygen and the production of reactive oxygen species (ROS).[7,8] Reactive oxygen species facilitate the production of toxic products and lead to the oxidation of cell membrane lipids.[9] Lipid peroxidation (LPO) caused through increased ROS as a result of hyperglycemia, has been shown to be important in the development of DM complications.[10] Moustafa et al reported that the amount of malondialdehyde (MDA), one of the LPO end products, increased significantly in the sciatic nerve tissue of rats with DM.[11] Galeshkalami et al have shown that hyperglycemia, which causes diabetic neuropathy, leads to the generation of ROS in neurons and their subsequent death They stated that increasing total antioxidant status (TAS) and glutathione (GSH) in neurons, and preventing the increase of ROS and LPO are associated with neuroprotection.[12] Solanki and Bhavsar revealed that the pain threshold decreased in diabetic rats having high oxidant levels and low antioxidant levels.[13] It has been revealed that neuropathy developing in diabetic rats causes significant hyperalgesia.[14] The acquired information suggest that antioxidants may be useful in the treatment of diabetic neuropathy and neuropathic pain. Research has focused on identifying alternative treatments with fewer side effects.[16]
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