Background: Huntington’s disease (HD) is a progressive neurodegenerative disease that causes motor, cognitive, and psychiatric abnormalities, with no satisfying disease-modifying therapy so far. 3-nitropropionic acid (3NP) induces behavioural deficits, together with biochemical and histological alterations in animals’ striata that mimic HD. The role of nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome in HD pathogenesis remains largely uncharacterized. Parthenolide (PTL), a naturally occurring nuclear factor kappa B (NF-κB) inhibitor, is also known to inhibit NLRP3 inflammasome. Whether PTL is beneficial in HD has not been established yet. Aim: This study evaluated the possible neuroprotective effects of PTL against 3NP-induced behavioural abnormalities, striatal biochemical derangements, and histological aberrations. Methods: Male Wistar rats received PTL (0.5 mg/kg/day, i.p) for 3 weeks and 3NP (10 mg/kg/day, i.p) was administered alongside for the latter 2 weeks to induce HD. Finally, animals were subjected to open-field, Morris water maze and rotarod tests. Rat striata were examined histologically, striatal protein expression levels of glial fibrillary acidic protein (GFAP), cluster of differentiation 45 (CD45) and neuron-specific enolase (NSE) were evaluated immunohistochemically, while those of interleukin (IL)-1β, IL-18, ionized calcium-binding adapter molecule-1 (Iba1) and glutamate were determined by ELISA. Striatal nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein (Keap1), NF-κB, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, S100 calcium-binding protein A10 (S100A10) and complement-3 (C3) were assessed by gene expression analysis. Results: PTL improved motor, locomotor, cognitive and anxiety-like behaviours, restored neuronal integrity, upregulated Nrf2, and inhibited NLRP3 inflammasome, NF-κB and microglial activation. Additionally, PTL induced astrocyte shifting towards the neuroprotective A2 phenotype. Conclusion: PTL exhibits neuroprotection against 3NP-induced HD, that might be ascribed, at least in part, to its modulatory effects on Keap1/Nrf2 and NF-κB/NLRP3 inflammasome signaling.

The current study aimed at investigating the potential hepatoprotective property and mechanism of meloxicam (MEL) against carbon tetrachloride (CCl₄)-induced hepatocellular damage in rats. Subcutaneous administration of CCl₄ (2 mL/kg, twice/week for 8 weeks) induced hepatocellular damage substantiated by hematoxylin and eosin staining and significant elevation in serum aspartate transaminase, alanine transaminase, and total bilirubin. In addition, CCL₄ treatment led to elevation in liver contents of lipid peroxidation marker (malondialdehyde), prostaglandin E2, active caspase 3, and Terminal deoxynucleotidyl transferase dUTP nick end labeling–positive cells and reduction in the activities of superoxide dismutase, catalase, glutathione- S-transferase, and reduced glutathione in the liver tissue. Prior oral treatment with MEL (5 mg/kg, twice/week) retained the normal liver histology and significantly restored all of these parameters close to normal values. These results demonstrated the hepatoprotective utility of MEL against the CCl₄-induced liver injury which might ascribe to its antioxidant, free radical scavenging, antiapoptotic and anti-inflammatory effects.

BACKGROUND: The gathered archeopathological evidence has confirmed that Schistosomiasis has been endemic in Ancient Egypt for over 500 decades. The association between Schistosoma hematobium and increase bladder cancer risk is also well acknowledged. However, over the years, there is a proved changing pattern of bladder cancer that needs to be investigated. AIM: We aim to discuss the truths and myths about bladder cancer and its association with Schistosomiasis in Egypt. METHODS: A cross-sectional, case-control study was performed to collect recent data on the topic. RESULTS: Of the reported cancer cases, 79.3% were transitional cell carcinoma (TCC), an additional 6% showed associated squamous features. Squamous cell carcinoma (SCC) constituted only 13.8% of cancer cases. Schistosomiasis was histologically confirmed in 19 cancer cases, only one was SCC. The relative frequency of TCC is increasing, while SCC is decreasing. There is no evidence that this pattern is related to smoking or environmental factors, as the incidence of lung cancer, is not proportionately increasing. CONCLUSION: The old concept that Schistosomiasis is associated with SCC should be revaluated as most cases are associated with TCC. Relying on the histopathology for confirmation of Schistosomiasis in our research studies appears to be non-accurate and leads to irrelevant results.