Objective: Intrapallidal inflammation may lead to the pathogenesis of Parkinson's disease. Pathological changes caused by lipopolysaccharide (LPS)-induced inflammation in Parkinson's disease rat models were largely unknown. Methods: Male Sprague-Dawley rat models were intra-globuspallidus injected with saline and lipopolysaccharide and divided into two groups, the control group and the LPS-stimulation group. The locomotor activity of the rat models was recorded for 4 consecutive weeks by trajectory analysis software for animal behavior. For the evaluation of pathological profiles, the expression levels of tyrosine hydroxylase and OX-42 in the substantia nigra tissues were detected by immunohistochemical staining. Also, the concentrations of dopamine at specific sites were detected through high-performance liquid chromatography. Perl's iron staining was used to evaluate iron accumulation in substantia nigra tissues. Results: LPS-stimulation reduced the locomotor capacity of the rat models compared with the control group. The density of tyrosine hydroxylase-positive cells was reduced and the secretion of striatal dopamine in the substantia nigra pars compacts was lower in the LPS group than it was in the control group. OX-42 positive microglia and ferritin levels were enhanced in the LPS group. Conclusion: Intrapallidal inflammation by LPS induced dopamine depletion and iron accumulation in the substantia nigra of Parkinson's disease rat models. The management of cerebral inflammation might be pivotal for PD pathogenesis and prognosis.