The protective effects of vitamin D (VitD) in different diseases were studied. The liver is of great interest, especially with the presence of VitD receptors. A high-fat diet (HFD) is associated with many diseases, including liver injury. Consumption of saturated fatty acids triggers hepatic apoptosis and is associated with increased inflammation. We aimed in this study to investigate the protective effects of VitD on hepatic molecular apoptotic changes in response to an HFD in rats. Forty male Wistar albino rats were used and divided into four groups: control, HFD, control + VitD, and VitD-supplemented HFD (HFD + VitD) groups. After six months, the rats were sacrificed, and the livers were removed. RNA was extracted from liver tissues and used for the quantitative real-time RT-PCR of different genes: B-cell lymphoma/leukemia-2 (BCL2), BCL-2-associated X protein (Bax), Fas cell surface death receptor (FAS), FAS ligand (FASL), and tumor necrosis factor α (TNF-α). The results showed that an HFD increased the expression of the pro-apoptotic genes Bax, FAS, and FASL, and reduced the expression of the anti-apoptotic gene BCL2. Interestingly, a VitD-supplemented HFD significantly increased the BCL2 expression and decreased the expression of all pro-apoptotic genes and TNFα. In conclusion, VitD has a protective role against hepatic molecular apoptotic changes in response to an HFD.

Fibromyalgia syndrome (FMS) is a chronic disorder marked by widespread musculoskeletal pain, fatigue, mood disturbances, and cognitive impairments. Current treatments primarily focus on symptom management. Ashwagandha (Withania somnifera), a traditional Ayurvedic herb, is known for its adaptogenic and neuroprotective properties. This study evaluated the protective effects of the methanolic root extract of Ashwagandha (ARE) in a reserpine-induced fibromyalgia model in male Swiss albino mice. Mice received oral ARE (100 mg/kg) for 17 days and reserpine (0.5 mg/kg, subcutaneously) for three consecutive days to induce fibromyalgia-like symptoms. Behavioral assessments included Von Frey, tail suspension, rotarod, and Y-maze tests. Histological analysis was conducted on the hippocampus and thalamus; however, neurochemical analysis focused on markers such as serotonin, norepinephrine, IL-1β, TNFα, MDA, and NO. Results indicated that ARE significantly reduced pain and depressive-like behavior and improved motor function (p < 0.0001); however, no significant changes were observed in open-field locomotion. Histological examination revealed protection of Ashwagandha against neurodegeneration and improved hippocampal integrity, accompanied by increased serotonin and norepinephrine levels and decreased pro-inflammatory cytokines. These findings suggest that Ashwagandha root extract may offer therapeutic benefits for managing fibromyalgia symptoms.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social communication and repetitive behaviors. Oxidative stress is increasingly recognized as a key contributor to the neuro-degeneration and behavioral abnormalities associated with ASD. Bacopa monnieri (BM), a medicinal herb with potent antioxidant and neuro-protective properties, has shown promise in mitigating oxidative damage. This study evaluated the preventive effects of BM extract on behavioral and neuro-histological alterations in a valproic acid (VPA)-induced mouse model of ASD. Pregnant mice received BM extract (400 mg/kg, orally) throughout gestation, while VPA (600 mg/kg) was administered intraperitoneally on embryonic day 12 (E12). Behavioral assessments included the open field test, righting reflex, three-chamber social interaction, marble burying, and hot plate tests. Oxidative stress markers, malondialdehyde (MDA) and glutathione (GSH), were quantified in hippocampal and cerebellar tissues. BM-treated offspring showed significant behavioral improvements, including reduced hyperactivity in the open field test (p < 0.0001), along with restored brain tissue architecture. Moreover, BM extract decreased MDA levels and elevated GSH concentrations, indicating attenuation of oxidative stress. In conclusion, Bacopa monnieri extract exerts protective effects against autism-like symptoms by enhancing antioxidant defenses and preserving neural integrity, suggesting its potential as a natural preventive strategy for ASD.

COVID-19 is a multisystem disease with important gastrointestinal (GI) involvement. Diarrhea, nausea or vomiting, reduced appetite, and abdominal pain are among the most frequently reported GI manifestations during acute infection, although their prevalence varies across populations, viral variants, disease severity, and study designs. The biological basis of intestinal involvement is supported by the expression of angiotensin-converting enzyme 2 (ACE2) and host proteases required for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry into intestinal epithelial cells. Viral RNA and antigens have also been detected in intestinal tissues after respiratory clearance, indicating persistence of viral material in some individuals; these findings do not by themselves demonstrate replication-competent virus. Uncommon but potentially severe GI complications include acute mesenteric ischemia, ischemic colitis, gastrointestinal bleeding, ileus, intestinal perforation, and acute pancreatitis. Although COVID-19 is associated with worse outcomes in acute pancreatitis, direct viral causation remains uncertain. Persistent GI manifestations have also emerged as an important component of post-COVID disease. Studies using Rome criteria have identified new-onset disorders of gut–brain interaction, including irritable bowel syndrome, functional dyspepsia, functional diarrhea, and functional constipation. Candidate mechanisms include intestinal viral antigen persistence, epithelial barrier dysfunction, sustained immune activation, gut microbial dysbiosis, and altered tryptophan–serotonin signaling; most links remain associative rather than causally established. Altered microbial signaling may also contribute to mucosal inflammation and disturbances in gut–lung and gut–brain communication. Overall, current evidence supports GI involvement in both acute and post-acute COVID-19. Further studies integrating microbiome, metabolic, and immune profiling are needed to clarify the mechanisms underlying post-COVID GI disorders and identify potential biomarkers and therapeutic targets.