| Retinal neurodegenerative disease invovled an inflammatory response in the retina characterized by increase in inflammatory cytokines and activation of microglia. The degree of microglia activation may influence the extent of retina injury following an inflammatory stimulus. Cytokines, released by activated microglia, regulate the influx of inflammatory cells to the damaged area. Thus, therapeutic strategy that reduces cytokine expression in microglia is known to be neuroprotective. Minocycline, a semisynthetic tetracycline derivative, protect brain against global and focal ischemia in rodents and inhibit microglial cell activation. To determine if minocycline can reduce the production of cytokines in microglia in response to Lipopolysaccharide (LPS), retina microglia cells were cultured in the presence or absence of 3 ng/ml of LPS. Semi-quantitative RT-PCR and Enzyme-linked immunosorbent assay (ELISA) were used to examine the changes in inflammatory cytokines, TNF alpha and IL-1beta. We also measured NO by nitrate reductase. TNF alpha, IL-1beta, and NO release from retinal microglia under LPS treatment was significantly higher and in a time-dependent means compared to untreated microglia. Minocycline inhibited these factors release from the LPS-stimulated retinal microglia. We conclude that LPS enhanced the inflammatory factors expression in cultured retinal microglia. Modulation of this expression was achieved with minocycline. Recognition of the mechanisms whereby minocycline exerts its anti-inflammatory effect on microglia may uncover specific targets for pharmacologic intervention. |
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