CX3CR1 mediates the neuroprotective effect of triptolide on 1-methyl-4-phenylpyridinium-induced hemiparkinson rats
ZHOU Zi-yi1, GAO Jun-peng2, XIANG Jun3, CHEN Yi-ping3, CAI Ye-feng1, LUO En-li1, CAI Ding-fang3
1. First Department of Neurology, Second Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120, China;
2. Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou 510180, China;
3. Laboratory for Neurological Research, The Institute of Integrative Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China
AIM: To investigate the effect of triptolide on the inhibition of microglial activation in 1-methyl-4-phenyl pyridinium (MPP+)-induced hemiparkinson disease rats.METHODS: The rat model of Parkinson disease was established by intranigral injection of MPP+. The rats were randomly divided into sham group, MPP+ group, triptolide group and vehicle group. The survival of dopaminergic neurons was detected by the immunofluorescence of tyrosine hydroxylase (TH) in the substantia nigra (SN). The activation of microglia was determined by immunofluorescence of OX-42 (microglia marker) in the SN. The expression of chemokine receptor CX3CR1 in SN was measured by Western blotting.RESULTS: Intranigral injection of MPP+ increased the fluorescence intensity of the microglial marker, and promoted DA neuron degenerative death. Immunohistological analysis showed that the OX-42 density was decreased (P<0.01) and tyrosine hydroxylase (TH) positive neurons were increased in the triptolide group (P<0.01). The expression of CX3CR1 was lower in triptolide group than that in model group (P<0.05).CONCLUSION: Triptolide may improve PA neurons function in MPP+-induced rats through inhibiting CX3CR1 expression and microglial activation.
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