Lipopolysaccharide (LPS), an endotoxin from Gram-negative bacteria, acts as a potent stimulator of microglia and has been\r\nused to study the inflammatory process in the pathogenesis of Parkinson�s disease (PD) and anti-inflammatory therapy for PD\r\ntreatment. Here, we review the growing body of literature on both in vitro and in vivo LPS PD models. Primary cell cultures from\r\nmesencephalic tissue were exposed to LPS in vitro; LPS was stereotaxically injected into the substantia nigra, striatum, or globus\r\npallidus of brain or injected into the peritoneal cavity of the animal in vivo. In conclusion, the LPS PD models are summarized\r\nas (1) local and direct LPS treatment and (2) systemic LPS treatment. Mechanisms underlying the PD models are investigated\r\nand indicated that LPS induces microglial activation to release a variety of neurotoxic factors, and damaged neurons may trigger\r\nreactive microgliosis, which lead to progressive dopaminergic neurodegeneration.
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