The Effect Of Electroacupuncture On Oxidative Damage And Neuroprotection After Status Epileticus In Rats

Temporal lobe epilepsy (TLE) is the most common subtype of epilepsy. One of the typical pathologic characteristics is neuronal damage in the hippocampus which is related to epileptogenesis. Oxidative stress may be one important reason to this. Antioxidative treatment might be helpful not only to protect neurons but also to inhibit epileptogenesis.Because both antiepileptic drugs and other treatments have many side effects, acupuncture becomes popular on account of safety and low cost. Acupuncture has been proven to have effect on epilepsy and oxidative stress in other diseases. It will be useful to figure out the efficacy of acupuncture on epileptogenesis and the mechanism of the neuroprotection.In this study,"Dazhui"and"Baihui"were chosen for electroacupuncture (EA)in lithium-pilocarpine model. The SD rats were assigned to four group: control group,electroacupuncture group,status epilepsy (SE) group and SE+EA group.The rats were treated everyday for a week before and after SE and the parameters of EA were adjusted properly according to our previous study. With biochemical detection, immunohistchemistry, immunofluorescence and Western blot, we tried to find out (1) whether EA can influence SE and spontaneous recurrent seizure (SRS); (2)whether EA can reduce neuronal damage in hippocampus after SE;(3)whether EA can inhibit oxidative stress after SE;(4)whether some neuroprotective path is activated by EA. The main findings are as follow,Although the duration and degree of SE were not changed, the frequencies and duration of SRS were inhibited by EA. This implies that acupuncturing the acupoints"Dazhui"and"Baihui"in lithium-pilocarpine model has anti- -epileptogenic effect. Neuronal loss in the subfields of hippocampus CA1, CA3 and hilus after SE were reduced after the treatment of EA which implies that EA has neuroprotecive effect after SE. Reactive oxygen species (ROS), MDA and heme oxygenase-1 (HO-1) were decreased while GSH and SOD activity were increased after EA which indicate it is through antioxidative stress that EA execuates its protective effects. With HO-1 antagonist SnPP, the mortality of SE rats increased and neuronal damage aggravated which show that HO-1 has neuroprotective effect after SE. PPARγwas increased after EA which indicates this might be the mechanism of neuroprotection of EA after SE.Taken together, in this study, EA is proven to inhibit oxidative damage after SE for the first time and reduce cell damage of hippocampus together with reduced SRS. It is found for the first time that EA can upregulate the expression of PPARγafter SE which might be the mechanism of the neuroprotective effect. The expressions of HO-1 and PPARγin the hippocampus after SE are also shown for the first time.