Diabetic foot is a serious complication of diabetes which has significant medical and socioeconomic impacts. Turmeric is a popular Indian spice that has been used for centuries in herbal medicines for the treatment of a variety of ailments such as rheumatism, diabetic ulcers, anorexia, cough and sinusitis. Curcumin is the main ingredient presents in turmeric and responsible for its yellow color. We report here a randomized, placebo-controlled investigation into the effectiveness of topical turmeric ointment in the treatment of diabetic foot ulcers. Seventy-six patients enrolled in the study. They were randomly divided into two groups, one of which received topical turmeric ointment and the other received placebo. Preparations were applied twice daily after irrigation of the wound by normal saline and dressed. Image analysis software was used to evaluate photographs of the ulcers and quantify the difference between treatment and placebo groups. Topical turmeric ointment demonstrated statistically significant reduction ( p < .001) in the size of diabetic ulcers at five weeks compared to placebo, independently of fasting blood sugar and HbA1C levels. Turmeric ointment may be an effective treatment for diabetic foot ulcers.
Introduction:Stimulation of peptidergic fibers activates microglia in the dorsal horn. Microglia activation causes fractalkine (FKN) release, a neuron-glia signal, which enhances pain. The transient vanilloid receptor 1 (TRPV1) mediates the release of neuropeptides, which can subsequently activate glia. TRPV1 and TRPV2 are generally expressed on C and Aδ fibers, respectively. Expression of both proteins is upregulated during inflammation, but expression of TRPV3 after induction of inflammation is unclear.Methods:Adult male Wistar rats were used in all experiments. Arthritis was induced in them by single subcutaneous injection of complete Freund’s adjuvant (CFA) in their right hindpaws. Resiniferatoxin (RTX) was used to eliminate peptidergic fibers. We examined the relation between FKN and TRPV3 expression by administration of anti-FKN antibody.Results:Our study findings indicated that 1) spinal TRPV3 was mostly expressed on nonpeptidergic fibers, 2) expression of spinal TRPV3 increased following inflammation, 3) elimination of peptidergic fibers decreased spinal TRPV3 expression, 4) alteration of hyperalgesia was compatible with TRPV3 changes in RTX-treated rat, and 5) anti-FKN antibody reduced spinal TRPV3 expression.Discussion:It seems that the hyperalgesia variation during different phases of CFA-induced arthritis correlates with spinal TRPV3 expression variation on peptidergic fibers. Moreover, spinal microglial activation during CFA inflammation is involved in TRPV3 expression changes via FKN signaling.
Introduction: Pain is an unpleasant sensory and emotional experience. Evidence suggests a role for microglia in chronic pain and inhibition of microglia leads to decrease of chronic pain intensity in animal models. Minocycline, a semisynthetic tetracycline derivative, is a selective inhibitor of microglia. Several studies have shown pain intensity improvement by minocycline in animal model of pain, but a few studies showed effectiveness on chronic pain improvement in humans. This prospective, self-controlled clinical trial investigated whether minocycline is effective for chronic pain management. Methods: Twenty-two patients, between the ages of 20 and 80 years with radicular lumbar pain with a numerical rating scale >4, who were unresponsive to other medications and had pain duration of >6 weeks were included in the trial. Results: Pain intensity, neuropathic pain and life quality scores assessed before and after treatment. All scores showed significant improvement after 2 weeks of treatment: 56%, 74% and 14%, respectively. Conclusion: Findings of this study suggest minocycline can effectively improve patients’ pain scores and quality of life, even in those with long-term duration of chronic pain and warrants further study.
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