Abstract
Purpose: To investigate the anti-neuroinflammatory effects of Isodon japonicus (Burm.) Hara extract (IJE) on BV2 microglial cells. .Methods: Cell viability was evaluated by MTT method. BV2 microglial cells were stimulated with lipopolyscarride (LPS, 1 μg/ml) and the effect of IJE on nitric oxide (NO) levels were measured using Griess assay. Immunoblot analysis was used to assess the effect of IJE on protein expression of inducible NO synthase (iNOS) expression. Tumor necrosis factor-alpha (TNF-α) cytokine production was evaluated by enzyme-linked immunosorbent assay (ELISA).Results: Pretreatment of 100 mg/ml of IJE (p < 0.001) was inhibited nitric oxide (NO) by 1 ug/ml LPStreated BV-2 cells. iNOS and TNF-α expression were attenuated by IJE concentration-dependently (p < 0.001 at 100 mg/ml). IJE scavenged 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radicals in a dosedependently with half-maximal inhibitory concentration (IC50) value of 46.5 μg/ml.Conclusion: Data from this study indicate that IJE attenuates neuroinflammatory responses. The strong anti-oxidant effect of IJE modulates expression of inflammatory molecules at the transcription level, and TNF-α at post-transcription level.Keywords: Isodon japonicas, Anti-oxidant, Neuroinflammation, BV-2 microglia, Nitric oxide
Highlights
Inflammation is often considered a universally harmful event
The increased expression of inducible NO synthase (iNOS) in activated BV-2 cells was suppressed at a concentration of 20 μg/ml and 40 μg/ml of Isodon japonicus (Burm.) Hara extract (IJE)
It is well accepted that activated microglia can produce various neurotoxic substances, including nitric oxide synthesized by iNOS mRNA expression
Summary
The presence of cytotoxic cytokines, invading immune cells, and tissue destruction reinforces the idea that inflammation is synonymous with tissue pathology. Neuroinflammation has been considered a driver of pathology and cognitive dysfunction for many years; not all inflammation results in the same outcome. The brain is sensitive to a wide variety of inflammatory stimuli that can result in different outcomes depending on the type of exposure, environment, and underlying pathological processes. Neuroinflammation is a result of an innate immune response in the CNS. Being a “semi-immune privileged organ” the brain and spinal cord have many resident cell types capable of producing immune related factors that can trigger neuroinflammation (1). Astrocytes, microglia, and even neurons are all crucial players in maintaining tissue homeostasis, and in times of pathology, each of these cell types can contribute to an
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