Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive motor and non-motor symptoms. PD neuropathology is due to the progressive deposition of mutant alpha-synuclein (α-Syn) in the dopaminergic neurons of the substantia nigra pars compacta (SNpc). This effect initiates oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis of the dopaminergic neurons in the SNpc. PD neuropathology, which is closely associated with inflammatory and oxidative disorders, disrupts different vital cellular pathways. Notably, the current anti-PD medications only relieve the symptoms of PD without averting the underlying neuropathology. Thus, it is advisable to search for novel drugs that attenuate the progression of PD neuropathology. It has been shown that phosphatidylinositol 3-kinase (PI3K), AKT, and glycogen synthase kinase 3 beta (GSK3β) signaling pathways are affected in PD. PI3K/AKT pathway is neuroprotective against the development and progression of PD. However, the over-activated GSK3β signaling pathway has a detrimental effect on PD neuropathology by inducing inflammation and oxidative stress. Dysregulation of the PI3K/AKT/GSK3β signaling pathway provokes brain insulin resistance (BIR), neuroinflammation, and neuronal apoptosis, the hallmarks of PD and other neurodegenerative diseases. However, the mechanistic role of the PI3K/AKT/GSK3β signaling pathway is not fully clarified. Therefore, in this review, we intend to discuss the role of the PI3K/AKT/GSK3β signaling pathway in PD pathogenesis and how PI3K/AKT activators and GSK3β inhibitors have helped effectively manage PD.

Background: Renal ischemia-reperfusion injury (IRI) is a significant contributor to renal dysfunction, acute kidney injury (AKI), and associated morbidity and mortality. Resveratrol, a polyphenol and phytoalexin, is known for its anti-inflammatory, antioxidant, and anti-cancer properties. This study investigates the nephroprotective potential of resveratrol in a rat model of renal IRI. Materials and methods: Twenty-eight male Sprague-Dawley rats were divided into four groups: Sham, IRI, DMSO, and Resveratrol. The Sham group underwent identical procedures without renal pedicle clamping, while the IRI group experienced 30 min of ischemia followed by 2 h of reperfusion. The DMSO group received dimethyl sulfoxide (DMSO) intraperitoneally 30 min before ischemia, and the Resveratrol group received 30 mg/kg resveratrol intraperitoneally 30 min before ischemia. Biochemical parameters (Urea, creatinine, IL-1β, NF-κβ, SOD, GSH, Bcl-2, and caspase-3) and histopathological changes were assessed. Results: IRI caused a substantial increase in serum creatinine, Urea, IL-1β, NF-κβ, and caspase-3 levels, while simultaneously decreasing SOD, GSH, and Bcl-2 levels. Resveratrol treatment mitigated these effects by lowering inflammatory and apoptotic markers, enhancing antioxidant defenses, and improving histological outcomes. Conclusion: Resveratrol demonstrates significant nephroprotective effects in renal IRI, primarily through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Objective and design: Prostatic inflammation is the driving force in benign prostatic hyperplasia (BPH). This work investigated the potential modulatory effect of COX-2 inhibition on ADAM-17/EGFR/ERK1/2 axis. Materials or subjects: Adult male Wistar rats were used. Treatment: Celecoxib (10 and 20 mg/kg; i.p.) was injected i.p. daily for three weeks. Testosterone (TST) (3 mg/kg; s.c.) was used to induce BPH. Methods: Prostatic inflammation and hyperplasia were assessed by organ weight and histopathology. Inflammatory mediators were measured using ELISA technique. Protein analysis was performed using western blotting and immunohistochemistry. Gene expression analysis was performed using qRT-PCR. Statistical analyses included one-way ANOVA and Tukey’s multiple comparison test. Results: Testosterone-treated rats had a marked increase in COX-2, prostate weight, and index. Moreover, TST-induced COX-2 was inferred from cytoskeletal changes and was attributable to the overexpression of PGE2, NF-κB (p65), and IL-6. COX-2-derived PGE2 increased the activity of ADAM-17, TGF-α, and TNF-α. Consequently, EGFR–ERK1/2 pathway was over-activated, disrupting anti-apoptotic Bcl-2, cyclin D1, and pro-apoptotic Bax. Celecoxib reversed these effects. Conclusion: COX-2 stimulates the ERK1/2 pathway via PGE2–ADAM-17-catalyzed shedding of TGF-α in testosterone-induced BPH. The results indicate a functional correlation between inflammation and hyperplasia in BPH.

The hydrothermal synthesis is presented of copper-doped carbon dots (Cu-CDs) from citric acid, urea, and copper chloride, resulting in blue-fluorescent particles with stable emission at 438 nm when excited at 340 nm. Through comprehensive spectroscopic and microscopic characterization (FTIR, XPS, UV, and HRTEM), the Cu-CDs demonstrated remarkable stability across varying pH levels, ionic strengths, temperatures, and UV exposure. Notably, Cu-CDs exhibit ultra-sensitive and selective detection of hexavalent chromium [Cr(VI)] ions in aqueous environments driven by fluorescence quenching. The system showed a robust linear response to Cr(VI) in the 0–80 µM range, with an impressive limit of detection (LOD) of 0.186 µM, significantly lower than the WHO’s permissible limit of 0.96 µM. These findings position Cu-CDs as an effective tool for environmental monitoring and water safety applications. Graphical Abstract