Intermittent Fasting Protects Against Age-Induced Rat Benign Prostatic Hyperplasia via Preservation of Prostatic Histomorphology, Modification of Oxidative Stress, and Beclin-1/P62 Pathway.

Intermittent fasting (IF) has several beneficial effects on most age-related degenerative changes in the body. Here we aimed to investigate the impact of IF on the biochemical and morphological abnormalities associated with normal aging in rat prostate. Thirty male albino rats were used and divided into three equal groups: adult group, rats aged 3 months; aged group, rats aged 15 months; and IF-aged group, rats aged 15 months maintained on intermittent fasting. After 3 months, prostates were excised and processed for biochemical, histological, and immunohistochemical study. Aging resulted in prostatic histological changes that resemble those of benign prostatic hyperplasia (BPH) with increased malondialdehyde (MDA) level, decreased glutathione (GSH) level, reduction of autophagy, and increased proliferation. Intermittent fasting ameliorated these described age-related prostatic changes. It could be concluded that IF could prevent age-induced BPH. This occurs via its anti-inflammatory and anti-proliferative effects, suppression of oxidative stress, and by improving autophagy via Beclin-1/P62 modulation. These mechanisms underlie the IF-mediated protection against age-related BPH. Because of IF safety and easy availability over BPH medications, it might be promising for managing BPH after further clinical studies.

Sacubitril/valsartan cardioprotective effect against cisplatin-induced cardiotoxicity via modulation of VEGF/eNOS and TLR4/TNFα/IL6 signalling pathways.

OBJECTIVES: Drug-induced cardiac injury is a potentially preventable cause of heart failure. Cisplatin (CIS) is a widely used chemotherapeutic agent complicated with cardiotoxicity that limits its clinical application so we aimed to evaluate the suspected cardioprotective effect of sacubitril/valsartan (Sac/Val) against CIS cardiotoxic injury. METHODS: Forty male rats of Wistar albino species were divided into four groups. group I received the vehicle; group II was given the vehicle plus CIS (10 mg/kg) single i.p. on fifth day; group III was given Sac/Val (30 mg/kg/d) orally for 7 days plus CIS (10 mg/kg) single i.p. on fif5th day; group IV was given the same as group III plus nitro-ω-L-arginine (L-NNA) (25 mg/kg/d) orally for 7 days. KEY FINDINGS: CIS-induced cardiotoxicity and L-NNA co-administered group showed significant increases in cardiac enzymes, toxic histopathological features, elevated heart weights, angiotensin II (Ang II), neprilysin, malondialdehyde (MDA), inflammatory mediators, blood pressure (BP) and caspase 3 expressions, but there are significant decreases in the antioxidant parameters, vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS). However, the co-administration of Sac/Val could ameliorate these changes of CIS. CONCLUSION: Sac/Val has an important cardioprotective effect against CIS cardiotoxicity with the involvement of eNOS.