The rising incidence of ischemic stroke poses significant health and healthcare burdens. Given the limitations of current therapeutic options, there is increasing interest in exploring the potential of galangin, a natural flavonoid compound, as a treatment for ischemic stroke. This study aimed to evaluate the neuroprotective effects and underlying mechanisms of galangin in mitigating oxidative stress, inflammation, and apoptosis in a rat model of permanent cerebral ischemia. Sixty male Wistar rats were divided into six groups: control; right middle cerebral artery occlusion (Rt.MCAO) with vehicle; Rt.MCAO with piracetam, a synthetic compound known as a cognitive enhancer; and Rt.MCAO with galangin administered at doses of 25, 50, and 100 mg/kg body weight. Neurological deficit scores, brain edema, neuronal density, and microglial morphology were assessed along with the activity of myeloperoxidase (MPO), a marker of inflammation, and superoxide dismutase (SOD). Additionally, the expression of key markers for inflammation and apoptosis, cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), Bcl-2-associated X protein (Bax), B-cell lymphoma-extra large (Bcl-XL), and caspase-3, was analyzed to elucidate potential mechanisms. The results demonstrated that galangin treatment significantly improved neurological deficit scores, reduced brain edema, enhanced neuronal density, attenuated microglial activation, decreased MPO activity, and increased SOD activity in both the cortex and hippocampus, highlighting its neuroprotective potential. These effects were linked to the modulation of inflammatory and apoptotic pathways. Specifically, galangin significantly reduced the expression of IL-6, COX-2, Bax, and caspase-3 while increasing the levels of the anti-apoptotic protein Bcl-XL. In conclusion, galangin demonstrates significant promise as a neuroprotective agent for ischemic stroke by suppressing inflammation and apoptosis, thereby improving neurological outcomes. However, clinical trials are required to validate these preclinical findings and confirm galangin’s therapeutic efficacy in humans.

Background/Objectives: Periductal fibrosis (PDF) is a common hepatobiliary abnormality associated with chronic Opisthorchis viverrini infection and may represent an ultrasonographic marker of chronic biliary injury in liver fluke-endemic regions. This systematic review and meta-analysis evaluated the association between ultrasound-defined PDF and cholangiocarcinoma (CCA)-related outcomes and summarized the prevalence of overall PDF and advanced periductal fibrosis (APF) in endemic populations. Methods: PubMed, Embase, and Scopus were searched from database inception to April 2026, supplemented by manual screening of reference lists. Observational studies reporting PDF prevalence and/or the association between PDF and CCA-related outcomes were included. Pooled odds ratios (ORs) and prevalence estimates were calculated using random-effects models. Five studies met the inclusion criteria. Results: Three studies involving 758,686 participants were included in the pooled association analysis. Ultrasound-defined PDF was associated with higher odds of CCA-related outcomes, including confirmed CCA, incident CCA, and clinically suspected CCA, with a pooled OR of 2.77 (95% CI: 2.24–3.44; I² = 0%). Because outcome definitions, effect measures, adjustment status, and PDF exposure categories varied across studies, this estimate should be interpreted as a summary association rather than as a precise estimate of confirmed CCA risk. Four studies involving 759,117 participants contributed to the overall PDF prevalence analysis, whereas three studies reported APF prevalence data. Prevalence estimates varied substantially across endemic settings, with extreme between-study heterogeneity. Conclusions: Overall, ultrasound-defined PDF may help identify individuals who warrant closer surveillance or further evaluation; however, it should not be interpreted as a definitive histopathological diagnosis or a proven causal precursor of CCA. Further prospective studies using standardized fibrosis definitions, blinded ultrasonographic assessment, confirmed or incident CCA outcomes, and adjustment for O. viverrini infection-related factors and other key confounders are needed to validate the role of PDF in CCA risk stratification.

Naringin is a naturally occurring flavanone glycoside found in citrus fruits that has been widely studied for its antioxidant and anti-inflammatory activities. The precise mechanisms by which naringin exerts protective effects against ischemic stroke are not yet fully understood. To address this gap, the current study examined the efficacy of naringin administration (100 mg/kg BW) in an experimental rat model involving permanent right middle cerebral artery occlusion (Rt.MCAO). Administration of naringin significantly improved neurological performance while reducing cerebral infarct volume and brain edema following ischemic injury. Histopathological evaluation further demonstrated that naringin preserved neuronal density in the cerebral cortex and hippocampus, indicating protection against ischemia-induced neuronal degeneration. In parallel, naringin attenuated glial activation, as evidenced by reduced expression of ionized calcium-binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP), accompanied by suppression of the pro-inflammatory mediators interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2). Furthermore, naringin restored redox homeostasis by lowering malondialdehyde (MDA) levels and preserving the activities of the endogenous antioxidant enzymes catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and mitochondrial superoxide dismutase (mitochondrial SOD). A significant reduction in myeloperoxidase (MPO) activity further supported its ability to alleviate oxidative stress and inflammatory responses. Our findings indicate that naringin has neuroprotective effects in experimental ischemic stroke. These effects were associated with improved antioxidant defenses and reduced neuroinflammatory responses. However, further preclinical studies are needed to confirm the underlying mechanisms, optimal treatment conditions, and long-term effects.