ABSTRACT
Objective To observe the effects of different energy of extracorporeal shock waves (ECSWs) on diabetic neuralgia in rats.Methods Fifty clean-grade healthy male Sprague-Dawley rats of both sexes,aged 8 weeks,weighing 180-200 g,were divided into 5 groups (n=10 each) using a random number table method:control group (group C),diabetic neuralgia group (group DN),low-energy ECSW group (group L + DN),medium-energy ECSW group (group M + DN),and high-energy ECSW group (group H+DN).Diabetic neuralgia models were established by intraperitoneally injecting streptozotocin (60 mg/kg) in DN,L+DN,M+DN and H+DN groups.ECSWs at 1,2 and 3 bar were applied during 4 consecutive weeks after successful establishment of the model once a week (T1-T4) in L+DN,M+DN and H+ DN groups,respectively.The mechanical paw withdrawal threshold (MWT),thermal paw withdrawal latency (TWL) and motor nerve conduction velocity (MNCV) were measured at T1-T4.Animals were sacrificed after the last measurement,and the sciatic nerve samples were obtained for determination of the expression of tumor necrosis factor-alpha (TNF-α) and interluekin-6 (IL-6) (by Western blot) and expression of TNF-α and IL-6 mRNA (by real-time polymerase chain reaction).Results Compared with group C,MWT,TWL and MNCV were significantly decreased at T1-T4,and the expression of TNF-α and IL-6 protein and mRNA was up-regulated in the other groups (P＜0.05).Compared with group DN,MWT at T2-4 and TWL and MNCV at T3,4 were significantly increased,and the expression of TNF-α and IL-6 protein and mRNA was down-regulated in L+DN,M+DN and H+DN groups (P＜0.05).Compared with group H+ DN,MWT at T2-4 and TWL and MNCV at T3,4 were significantly increased,and the expression of TNF-α and IL-6 protein and mRNA was down-regulated in L+DN and M+DN groups,and the expression of IL-6 mRNA was significantly down-regulated in group L+DN (P＜0.05).Conclusion ECSWs can mitigate diabetic neuralgia in rats,and the low-and medium-energy ECSWs produce better efficacy,and the mechanism is related to inhibiting inflammatory responses.