Diacerein provokes apoptosis, improves redox balance, and downregulates PCNA and TNF-α in a rat model of testosterone-induced benign prostatic hyperplasia: A new non-invasive approach.

One of the most prevalent chronic conditions affecting older men is benign prostatic hyperplasia (BPH), causing severe annoyance and embarrassment to patients. The pathogenesis of BPH has been connected to epithelial proliferation, inflammation, deranged redox balance, and apoptosis. Diacerein (DIA), the anthraquinone derivative, is a non-steroidal anti-inflammatory drug. This study intended to investigate the ameliorative effect of DIA on the prostatic histology in testosterone-induced BPH in rats. BPH was experimentally induced by daily subcutaneous injection of testosterone propionate for four weeks. The treated group received DIA daily for a further two weeks after induction of BPH. Rats' body and prostate weights, serum-free testosterone, dihydrotestosterone, and PSA were evaluated. Prostatic tissue was processed for measuring redox balance and histopathological examination. The BPH group had increased body and prostate weights, serum testosterone, dihydrotestosterone, PSA, and oxidative stress. Histologically, there were marked acinar epithelial and stromal hyperplasia, inflammatory infiltrates, and increased collagen deposition. An immunohistochemical study showed an increase in the inflammatory TNF-α and the proliferative PCNA markers. Treatment with DIA markedly decreased the prostate weight and plasma hormones, improved tissue redox balance, repaired the histological changes, and increased the proapoptotic caspase 3 expression besides the substantial reduction in TNF-α and PCNA expression. In conclusion, our study underscored DIA's potential to alleviate the prostatic hyperplastic and inflammatory changes in BPH through its antioxidant, anti-inflammatory, antiproliferative, and apoptosis-inducing effects, rendering it an effective, innovative treatment for BPH.

Histological Study on the Protective Role of Ascorbic Acid on Cadmium Induced Cerebral Cortical Neurotoxicity in Adult Male Albino Rats.

Cadmium (Cd) toxicity represents a worldwide problem in environmental contamination and a common cause of occupational and non-occupational neurological diseases. So, this study aimed to evaluate the histological changes induced by Cd on the cerebral cortex of adult rats and evaluating the possible ameliorating role of ascorbic acid (AA). Twenty adult male rats were divided into; control group, AA group (each rat was received a daily oral dose of 200 mg AA/kg body weight (b.w) and Cd group (each rat was received 5 mg Cd/kg b.w orally) and protective group (each rat was given AA concomitantly with Cd at the same dose, route and period of administration of the previous groups. After two months the cerebral cortexes were processed for histological examination. The cerebral cortex of Cd treated animals exhibited severe degenerative changes especially in pyramidal and granule cells. Structural changes in these cells were in the form of dilated rER and Golgi complex, swollen mitochondria and marginated nuclear chromatin. Myelinated nerve fibers displayed myelination disruption and irregular neurofilaments. The neuropil appeared vacuolated with accumulation of neuroglial cells. On the other hand, these changes were ameliorated in rats which received AA concomitantly with Cd. So, it could be concluded that AA can ameliorate the histological changes induced by Cd and this direct the attention to the antioxidants as protective measures for the neurotoxicity.