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Background: Diabetic neuropathy is a debilitating manifestation of long-term diabetes mellitus. The present study explored the effects of the roots of Rubia cordifolia L. (R. cordifolia L.) in the Wistar rat model for diabetic neuropathy and possible neuroprotective, antidiabetic, and analgesic mechanisms underlying this effect. Materials and Methods: Rats were divided into five experimental groups. An amount of 0.25% carboxy methyl cellulose (CMC) in saline and streptozotocin (STZ) (60 mg/kg) was given to group 1 and group 2, respectively. Group 3 was treated with STZ and glibenclamide simultaneously while groups 4 and 5 were simultaneously treated with STZ and hydroalcoholic extract of the root of R. cordifolia, respectively. Hot plate and cold allodynias were used to evaluate the pain threshold. The antioxidant effects of R. cordifolia were assessed by measuring Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). At the end of the study, sciatic nerve and brain tissues were collected for histopathological study. Bcl-2 proteins, cleaved caspase-3, and Bax were assessed through the Western blot method. Results: R. cordifolia significantly attenuated paw withdrawal and tail flick latency in diabetic neuropathic rats. R. cordifolia significantly (p < 0.01) improved the levels of oxidative stress. It was found to decrease blood glucose levels and to increase animal weight in R. cordifolia-treated groups. Treatment with R. cordifolia suppressed the cleaved caspase-3 and reduced the Bax:Bcl2 ratio in sciatic nerve and brain tissue compared to the diabetic group. Histopathological analysis also revealed a marked improvement in architecture and loss of axons in brain and sciatic nerve tissues at a higher dose of R. cordifolia (400 mg/kg). Conclusion: R. cordifolia attenuated diabetic neuropathy through its antidiabetic and analgesic properties by ameliorating apoptosis and oxidative stress. [ABSTRACT FROM AUTHOR]

Objectives: Pitavastatin is a competitive HMG-CoA reductase inhibitor for lowering of cholesterol level and low density lipoprotein cholesterol. This study was designed to evaluate the effect of pitavastatin in neuropathic pain induced by partial sciatic nerve ligation along with neuronal changes in Wister rats. Methods: Pitavastatin was started three days prior to the surgery and continued for 14 days The pain was determined by thermal hyperalgesia and cold allodynia. The biochemical changes were estimated at the end of the study. The levels of cytokines were measured using an ELISA test. Western blot analysis was used to detect levels of expression of JNK, p-JNK, ERK, p-ERK, p38MAPK, p-p38MAPK. The sciatic nerve was investigated histopathologically. Key findings: Pitavastatin significantly ameliorated nerve pain induced by PSNL and also attenuated the biochemical changes in a dose-dependent manner. The levels of inflammatory mediators were inhibited by pitavastatin. There was significant improvement in sciatic nerve fibres histology. The levels of p-38, p-ERK, and p-JNK and their associated phosphorylated proteins were reduced after treatment with pitavastatin. Conclusion: The present study indicates that treatment with pitavastatin reversed the PSNL-induced neuropathy in Wister rats and may be an additional therapeutic strategy in the management of neuropathic pain. [ABSTRACT FROM AUTHOR]