Some evidence suggests glial-mediated inflammation as a possible origin for Parkinson's disease via activation of microglia that release nitric oxide, proteases, and proinflammatory cytokines (105). Feng-Qiao et al. made the interesting observation that triptolide concentration dependently attenuated lipopolysaccharide-induced decrease in [3H] dopamine uptake and loss of tyrosine hydroxylase-immunoreactive neurons in primary mesencephalic neuron/glia mixed culture (106). This result suggests that triptolide may protect dopaminergic neurons from lipopolysaccharide-induced degeneration.

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