curcumin and Sciatica

RUNX Family Transcription Factor 2 (Runx2) promotes neurite outgrowth after sciatic nerve injury, and Curcumin can promote the expression of Runx2. It is worthwhile to explore whether curcumin's repair effect on sciatic nerve injury is related to Runx2.. To investigate the repair effect of curcumin on sciatic nerve injury and its possible mechanism.. Curcumin improved the sciatic functional index (SFI) and toe spread index (TSI) of rats with sciatic nerve injury and increased the number and diameter of myelinated axons in the sciatic nerve. Curcumin promoted the myelination of SCs (Schwann cells) by increasing the expression of peripheral myelin protein 22 (PMP22), fibrin, S100, and proliferating cell nuclear antige (PCNA). Curcumin treatment increased the proliferation of SCs and the expression of Runx2. Cell experiments further confirmed that curcumin promoted Schwann cell proliferation and myelination through Runx2.. Curcumin promotes SCs proliferation and myelination through Runx2 and improves sciatic nerve repair.

Topics: Animals; Cell Line; Cell Proliferation; Core Binding Factor Alpha 1 Subunit; Curcumin; Fibrin; Male; Myelin Proteins; Myelin Sheath; Nerve Regeneration; Neuroprotective Agents; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; S100 Proteins; Schwann Cells; Sciatica

Neuropathic pain is a debilitating chronic pain condition, and its treatment remains a clinical challenge. Curcumin, a naturally occurring phenolic compound, possesses diverse biological and pharmacological effects but has not yet been approved as a drug due to its low bioavailability. In order to overcome this limitation, we synthesized a potential ester prodrug of curcumin, curcumin diethyl diglutarate (CurDDG). In this study, we evaluated the pharmacological advantages of CurDDG over curcumin in a mouse model of chronic constriction injury (CCI), and the anti-inflammatory effect of CurDDG in LPS-induced RAW 264.7 macrophage cells was accessed to clarify the underline mechanism. Mice were treated with various oral doses of curcumin (25, 50, 100 and 200 mg/kg/day, daily for 14 days) or equimolar doses of CurDDG. CurDDG at all doses tested significantly attenuated CCI-induced thermal hyperalgesia and mechanical allodynia compared with the CCI-control group. CurDDG at 25, 50 and 100 mg/kg demonstrated significantly greater efficacy on both mechanical and thermal hypersensitivities compared to that of curcumin. The effect of CurDDG correlated well with the inhibition of TNF-α and IL-6 levels in both the sciatic nerve and the spinal cord, as compared to its respective control groups. Similarly, in the in vitro study, CurDDG significantly reduced the LPS-induced expression of TNF-α and IL-6. Moreover, CurDDG significantly decreased COX-2 and iNOS levels and attenuated p38, JNK, and ERK1/2 phosphorylation as compared to the curcumin-treated cells. Altogether, this study demonstrated the improved pharmacological effects of curcumin by its diglutarate conjugate, CurDDG.

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Behavior, Animal; Curcumin; Cyclooxygenase 2; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Glutarates; Hyperalgesia; Inflammation Mediators; Interleukin-6; Macrophages; Male; Mice; Mice, Inbred ICR; Nitric Oxide Synthase Type II; Pain Threshold; Phosphorylation; Prodrugs; RAW 264.7 Cells; Sciatic Nerve; Sciatica; Signal Transduction; Spinal Cord; Succinates; Tumor Necrosis Factor-alpha

Curcumin exhibits a wide spectrum of biological activities which include neuroprotective, antinociceptive, anti-inflammatory, and antioxidant activity.. The present study evaluates the effect of curcumin in vincristine-induced neuropathy in a mice model.. Vincristine sulfate (0.1 mg/kg, i.p. for 10 consecutive days) was administered to mice to induce neuropathy. Pain behavior was assessed at different days, i.e., 0, 7, 10, and 14 d. Sciatic nerve total calcium, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), nitric oxide (NO), and lipid peroxidation (LPO) were also estimated after the 14th day of study. Pregabalin (10 mg/kg, p.o.) and curcumin (15, 30, and 60 mg/kg, p.o.) were administered for 14 consecutive days.. Curcumin at 60 mg/kg significantly attenuated the vincristine-induced neuropathic pain manifestations in terms of thermal hyperalgesia (p < 0.001) and allodynia (p < 0.001); mechanical hyperalgesia (p < 0.001); functional loss (p < 0.001); and in the delayed phase of formalin test (p < 0.001). Curcumin at 30 and 60 mg/kg exhibited significant changes (p < 0.001) in antioxidant levels and in total calcium levels in vincristine-injected mice.. Curcumin at 30 and 60 mg/kg dose levels significantly attenuated vincristine-induced neuropathy which may be due to its multiple actions including antinociceptive, calcium inhibitory, and antioxidant effect.

Topics: Animals; Antineoplastic Agents, Phytogenic; Antioxidants; Behavior, Animal; Calcium; Calcium Channels, N-Type; Curcumin; Male; Mice; Neuralgia; Neuroprotective Agents; Pain Measurement; Peripheral Nervous System Diseases; Postural Balance; Sciatica; Vincristine