Bisphenol A-induced polycystic ovary syndrome (PCOS) with hormonal and metabolic implications in rats.

There is a rising incidence of polycystic ovary syndrome (PCOS) cases worldwide in women of reproductive age due to environmental factors. We evaluated the effect of an environmental estrogen, bisphenol A (BPA) for its reprotoxicity regarding the induction of PCOS in rats and also assessed its hormonal and metabolic implications. There was 66.

Obesity aggravates neuroinflammatory and neurodegenerative effects of bisphenol A in female rats.

Bisphenol A (BPA), a common plasticizer, is categorized as a neurotoxic compound. Its impact on individuals exhibits sex-linked variations. Several biological and environmental factors impact the degree of toxicity.

Downregulation of ATF-4 Attenuates the Endoplasmic Reticulum Stress-Mediated Neuroinflammation and Cognitive Impairment in Experimentally Induced Alzheimer's Disease Model.

Protein aggregation is invariably associated with the inflammation as a factor in Alzheimer's disease (AD). We investigated the interaction between downstream factors of endoplasmic reticulum (ER) stress pathway and inflammation, with implications in cognitive impairment in AD. Amyloid-β (Aβ) was administered by bilateral intracerebroventricular (icv) injection in the brain of adult male Wistar rats to experimentally develop AD.

Tempol (4-hydroxy tempo) protects mice from cisplatin-induced acute kidney injury modulation of expression of aquaporins and kidney injury molecule-1.

Tempol (4-hydroxy tempo), a pleiotropic antioxidant is reported to afford protection against cisplatin (CP)-induced nephrotoxicity. However, molecular mechanisms of action of tempol in improving the renal function in CP-induced nephrotoxicity are not fully understood. We investigated the attenuating effect of tempol against CP-induced alterations in kidney injury molecule-1 (KIM-1) and aquaporins (AQPs) in mice.

Involvement of endoplasmic reticulum stress in amyloid β -induced Alzheimer's like neuropathological process in rat brain.

Amyloid-β (Aβ) accumulation in the brain is a pathological hallmark of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress has been implicated in aetiology of neurodegenerative disorders. We studied the involvement of ER stress in Aβ-induced neuronal degeneration in rat brain to correlate it with cellular and molecular modifications in Aβ-induced Alzheimer's like neuropathological process.