Microglial Neuroinflammation-Independent Reversal of Demyelination of Corpus Callosum by Arsenic in a Cuprizone-Induced Demyelinating Mouse Model.

Demyelination is the loss of myelin in CNS, resulting in damaged myelin sheath. Oxidative stress and neuroinflammation play a key role in inducing demyelinating diseases like MS; hence, controlling oxidative stress and neuroinflammation is important. Cuprizone (CPZ), a copper chelator, generates oxidative stress and neuroinflammation, thereby inducing demyelination.

Perinatal arsenic exposure-induced sustained microglial activation leads to impaired cognitive response in BALB/c mice.

Arsenic is infamous for its adverse health effects worldwide. It is known to induce cognitive impairment in experimental model animals and children in the arsenic-affected area. Although the effect of arsenic on neuronal health is well studied, but the involvement of the brain immune component, microglia, has not been well explored.

A study on bisphenol S induced nephrotoxicity and assessment of altered downstream kidney metabolites using gas chromatography-mass spectrometry based metabolomics.

The global use of bisphenol S (BPS) has now been significantly increased for commensurate utilization as a substitute for BPA for its regulatory concerns. Though, previous reports indicated that BPS been also appeared as a toxic congener comparable to BPA. In the present study, we determined nephrotoxicity condition induced due to BPS exposure.

Minocycline reverses developmental arsenic exposure-induced microglia activation and functional alteration in BALB/c mice.

Arsenic activates microglia and exerts bystander effects on neuron. The present study is focused to test whether minocycline, a second generation antibiotic, can reverse the effect of developmental arsenic exposure on microglial activation and function. Pregnant Balb/c dams were gavaged with sodium arsenite (0.

MicroRNA-129-5p-regulated microglial expression of the surface receptor CD200R1 controls neuroinflammation.

CD200R1 is an inhibitory surface receptor expressed in microglia and blood macrophages. Microglial CD200R1 is known to control neuroinflammation by keeping the microglia in resting state, and therefore, tight regulation of its expression is important. CCAAT/enhancer-binding protein β (CEBPβ) is the known regulator of CD200R1 transcription.

Metabolomic perturbation precedes glycolytic dysfunction and procreates hyperglycemia in a rat model due to bisphenol S exposure.

Previous studies highlighted bisphenol S (BPS), an industrial chemical responsible for harmful effects comparable to its congener substance bisphenol A (BPA). Accounted for various adversities to biological functions, it could alter the expression of endogenous metabolites in many metabolic processes. The study was aimed to investigate the altered metabolites in hyperglycemic condition triggered by sub-chronic exposure of BPS in serum and urine samples of Wistar rats.

Correction to: Sneaky Entry of IFNγ Through Arsenic-Induced Leaky Blood-Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine.

The original version of this article unfortunately contained mistake on Fig. 3A.

Sneaky Entry of IFNγ Through Arsenic-Induced Leaky Blood-Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine.

Recent studies showed that neuronal surface protein CD200 plays a key role in the regulation of neuroinflammation. Previously, we showed that arsenic (0.38 mg/kg body weight) exposure induces microglial activation and consequently IL-6/TNF-α secretion.