Effect of intrathecal cardamonin on diabetic neuropathic pain in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of intrathecal cardamonin on diabetic neuropathic pain (DNP) in rats.Methods Healthy adult male Sprague-Dawley rats,aged 2 months,weighing 180-220 g,were included in the study.Diabetes mellitus was produced by intraperitoneal injection of streptozotocin 60 mg/kg after intrathecal catheterization.When decrease in pain threshold＞50％ of the baseline at 21 days after diabetes mellitus was produced,the induction of DNP was considered successful.Twenty-four rats with DNP were divided into 4 groups (n=6 each) using a random number tablegroup DNP,rapamycin group (group R),cardamonin 50 μg group (group D50) and cardamonin 100 μg group (group D100).Another 6 healthy age-matched rats were used as normal control (group C).In DNP,R,D50 and D100 groups,dimethyl sulfoxide 10 μl,rapamycin 5 μg and cardamonin 50 μg and 100 μg were intrathecally injected,respectively,once a day for 7 consecutive days starting from 21 days after successful estabiishment of the model.Mechanical paw withdrawal threshold (MWT) was measured before establishment of the model,on 7,14 and 21 days after establishment of the model,and on 1,4 and 7 days after intrathecal injection.The rats were sacrificed after the last MWT measurement,and their L3-5 segments of the spinal cord were removed for determination of the expression of S6K,p-S6K and synapsin Ⅱ by Western blot.Results Compared with group C,MWT was significantly decreased,and the expression of spinal S6K,p-S6K and synapsin Ⅱ was up-regulated in group DNP (P＜0.05 or 0.01).Compared with group DNP,MWT was significantly increased,and the expression of spinal S6K,p-S6K and synapsin Ⅱ was down-regulated in R,D50 and D100 groups (P＜0.05 or 0.01).Compared with group D50,MWT was significantly increased,and the expression of spinal S6K,p-S6K and synapsin Ⅱ was down-regulated in group D100 (P＜0.05).Conclusion Intrathecal cardamonin can relieve DNP in rats,and the mechanism is related to inhibiting spinal mammalian target of rapamycin activity and down-regulating the expression of synapsin Ⅱ.