Effect of naringin on gp120-induced injury mediated by P2X7 receptors in rat primary cultured microglia.
Qiang ChenHui WuJia TaoChenglong LiuZeyu DengYang LiuGuoqiao ChenBaoyun LiuChangshui XuPublished in: PloS one (2017)
Human immunodeficiency virus type-1 (HIV-1) envelope glycoprotein 120 has been shown to activate microglia, causing release of inflammatory and toxic factors. The P2X7 receptor, primarily expressed on microglia, is closely associated with inflammation. Naringin, a plant bioflavonoid, has anti-inflammatory and anti-oxidative properties. We hypothesized that P2X7 receptor mediated gp120-induced injury in primary cultured microglia, and that naringin would have a protective effect. We showed that HIV-1 gp120 peptide (V3 loop, fragment 308-331) appeared to induce apoptosis of primary cultured microglia. However, there was a decrease of microglia apoptosis in gp120+naringin group compared with gp120 group. Using qPCR, Western blot, and immunofluorescence, we showed that gp120 stimulated expression of P2X7 mRNA and receptor protein, and this stimulation was inhibited by naringin. Treatment with gp120 increased concentrations of eATP, TNFα and IL-1β, and these effects were inhibited by naringin. Taken together, these results suggested that gp120 contributed to microglial cell injury and neurotoxic activity by up-regulating expression of P2X7, in a naringin-protective manner.
Keyphrases
- human immunodeficiency virus
- inflammatory response
- oxidative stress
- neuropathic pain
- antiretroviral therapy
- hepatitis c virus
- hiv infected
- hiv positive
- endothelial cells
- poor prognosis
- diabetic rats
- high glucose
- hiv aids
- south africa
- lipopolysaccharide induced
- cell death
- signaling pathway
- stem cells
- spinal cord
- lps induced
- cell therapy
- bone marrow
- mesenchymal stem cells
- pi k akt