Shakir D AlSharari1,
Salim S Al-Rejaie1 
,
Hatem M Abuohashish1,2,
Abdulaziz M Aleisa1,
Mihir Y Parmar1,
Mohammed M Ahmed1
For correspondence:- Salim Al-Rejaie Email: rejaie@hotmail.com Tel:+9661146771787
Received: 15 May 2014 Accepted: 4 August 2014 Published: 24 September 2014
Citation: AlSharari SD, Al-Rejaie SS, Abuohashish HM, Aleisa AM, Parmar MY, Ahmed MM. Ameliorative Potential of Morin in Streptozotocin-Induced Neuropathic Pain in Rats. Trop J Pharm Res 2014; 13(9):1429-1436 doi: 10.4314/tjpr.v13i9.8
© 2014 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Purpose: To investigate the protective effect of morin, a naturally occurring bioflavonoid of Moraceae family, in experimentally-induced diabetic neuropathy (DN) in rats.
Methods: Diabetes was induced by a single injection (65 mg/kg, ip) of streptozotocin (STZ). Morin (15 and 30 mg/kg/day) oral treatment was started 3 weeks after diabetes induction and continued for 5 consecutive weeks. Pain threshold behavior tests were performed at the end of the treatment. In sciatic nerve, inflammatory cytokines (TNF-α, IL-1β, IL-6), nerve growth factor (NGF) and insulin growth factor (IGF-1) were determined using ELISA kits, while thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels were assessed.
Results: Diabetic animals showed apparent decreased paw-withdrawal (39 %, p < 0.05) and tail-flick (31 %, p < 0.05) latency as compared with control group. All the measured biomarkers were altered (p < 0.05 to 0.001) in diabetic rats compared with control non-diabetic animals. Morin treatment attenuated hyperalgesia and analgesia (p < 0.05) respectively. Morin treatment of diabetic rats at both doses significantly decreased the levels of cytokines (p < 0.01), glucose (p < 0.01) and TBARS (p < 0.001), but increased NGF (p < 0.01), IGF-1 (p < 0.01) and GSH (p < 0.01) levels in sciatic nerves compared to untreated diabetic animals. Inhibited activities (U/mg protein) of SOD (1.08 ± 0.16) and CAT (2.77 ± 0.36) in sciatic nerve of diabetic rats also found corrections (2.09 ± 0.11, p < 0.01) and (4.53 ± 0.57, p < 0.01) after morin (30 mg/kg/day) treatment, compared with untreated diabetic animals.
Conclusion: These findings demonstrate the protective effect of morin mediated through reduction of oxidative stress and inflammatory process, and suggest the therapeutic potential of morin in the attenuation of diabetic neuropathy.
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