currently, microglia are considered as crucial factors in suppressing inflammatory reactions, but the specific molecular mechanism remains unknown. To elucidate whether peroxisome proliferator-activated receptor-γ (PPar-γ) can inhibit neuroinflammatory cytokine expression via the mTOR signal pathway, the BV-2 cell line was incubated with lipopolysaccharide (10 mM/ml) to induce an inflammatory injury. PPAR-γ was activated by rosiglitazone, and was inhibited by GW9662. The mTOR signal pathway was activated by phosphatidic acid (P.A.), while it was inhibited by rapamycin. Western blotting and reverse transcription-quantitative PCR were used to evaluate the expression levels of PPAR-γ/mTor signal pathway related proteins and neuroinflammatory cytokines, including NF-κB, tumor necrosis factor (TNF)-α and interleukin (IL)-1β. When treated with P.A., the expression levels of phosphorylated (p)mTOR and p-ribosomal protein S6 kinase (pS6K) were significantly increased and the expression levels of TNF-α and il-1β were significantly lower. However, the expression of PPAR-γ was similar in P.A. treated cells and cells treated with rapamycin. When PPAR-γ was activated, pmTOR and pS6K protein expression levels were significantly decreased, and the mRNA expression levels of TNF-α and il-1β were significantly reduced, but this inhibition could be alleviated by administrating GW9662. Collectively, it was indicated that the mTOR signal pathway may be located downstream of PPar-γ. Furthermore, neuroinflammatory reactions could be inhibited via the activation of PPAR-γ by suppressing the mTOR signal pathway in microglia.