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Omid Dastgerdi, Ahmad Kaki,
Volume 20, Issue 2 (1-2021)
Abstract

Background: Neuroinflammation and oxidative stress play a pivotal role in the diabetic neuropathic pain. The aim of this study was to evaluate the effect of aerobic exercise with melatonin on RAGE gene expression and some indicators of oxidative stress in rats with diabetic neuropathic pain
Methods: Forty 8-week-old male Wistar rats (weight range 204 ± 11.3 g) were randomly divided into five of 8 groups including: diabetic neuropathy (50 mg / kg streptozotocin intraperitoneal injection), diabetic melatonin neuropathy (mg / kg 10 melatonin daily for 6 weeks), diabetic neuropathy exercise (30 minutes of aerobic exercise at 15 meters per minute, 5 days a week for 6 weeks), diabetes melatonin neuropathy and healthy exercise and control. After confirmation of diabetic neuropathy by behavioral tests, exercise protocol and supplementation were performed. RAGE gene expression was measured by real-time technique and oxidative stress indices in spinal cord tissue by spectrophotometer. One-way analysis of variance and Tukey's post hoc test were used for statistical analysis.
Results: Exercise and melatonin reduced the sensitivity of the nervous system to thermal hyperalgesia and mechanical allodynia. Aerobic exercise with melatonin significantly reduced RAGE gene expression and MAD concentration and increased the activity of SOD and CAT enzymes compared to the diabetic neuropathy group (P <0.05).
Conclusion: Aerobic exercise with melatonin modulates the expression of RAGE gene and oxidative stress indices and improves the sensitivity of nociceptors to pain factors. It is recommended to use aerobic exercise with melatonin for diabetics to reduce neuropathic pain.
Akram Batvandi, Ahmad Kaki,
Volume 21, Issue 4 (10-2021)
Abstract

Background: Dysfunction of Schwann cells by diabetes has far-reaching consequences for the structure and function of peripheral nerves. The aim of the present study was to evaluate the effect of aerobic exercise on the Nrg1 / ErbB2 signaling pathway in male rats with diabetic neuropathic pain.
Methods: Twenty-four 8-week-old male Wistar rats (weight range 204 ± 11.3 g) were randomly divided into three groups (n = 8) including: Diabetic neuropathy (50 mg / kg streptozotocin injection), Diabetic neuropathy Exercise (30 minutes exercise aerobics intensity 15 m/min, 5 days per week for 6 weeks), and healthy controls. After confirmation of diabetic neuropathic pain by behavioral tests, aerobic exercise protocol was performed. The expression of Nrg1 / ErbB2 genes was measured by real-time technique. One-way analysis of variance and Tukey's post hoc test were used for statistical analysis.  
Results: Aerobic exercise reduced the nervous system's sensitivity to thermal hyperalgesia and mechanical allodynia. Induction of diabetes significantly reduced Nrg1 and ErbB2 gene expression. There was also a significant increase in the expression of the above genes in the exercise group compared to the diabetic neuropathy group (P<0.05).
Conclusion: It seems that aerobic exercise is effective in increasing the nerve repair process by activating growth signaling pathways in Schwann cells. It is recommended that aerobic exercise be used for diabetics to reduce neuropathic pain.

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