Objectives: Methotrexate (MTX) is an anticancer drug used in chemotherapy. MTX was known for its toxic effects involving most of the organs including testis. Bee pollen is healthy food for human and has antioxidant effect. We intended to determine protective effect of bee pollen against testicular injury caused by MTX in rats. Methods: Thirty-two adult Sprague Dawley male rats were used, and 4 groups were formed: control, MTX, pollen, and MTX + pollen. Rats were given pollen at a dose of 400 mg/kg with intragastric gavage for 10 days. On day 7, MTX was administered a single dose of 30 mg/kg ip. Serum testosterone and LH, tissue MDA level, and SOD and CAT enzyme activities were examined. In addition, spermatological parameters were evaluated. Results: MDA level and SOD activity increased while testosterone level decreased significantly in the MTX group compared to the control group. In the MTX + pollen group, MDA level and SOD activity decreased while testosterone level increased. There was no significant change in CAT activity and LH values. Abnormal sperm ratio decreased in the MTX + pollen group compared to the MTX group. Conclusions: Our results suggest that bee pollen has a healing effect on reproductive parameters in testicular damage caused by MTX.

Objective: The antidepressant agomelatine agent is a melatonin receptor (MT1 and MT2) agonist and a serotonin receptor (5-HT2C) antagonist. Increasing evidence shows that agomelatine has neuroprotective and neuromodulatory effects. In this study, the potential effects of agomelatine in rats with scopolamine-induced cognitive impairment were investigated.Materials and Methods: Adult male rats were administered scopolamine (1 mg/kg) and agomelatine (40 mg/kg) for 21 days. After drug administration, rats were subjected to new object recognition (NOR) and Morris water maze (MWM) tests in order to evaluate cognitive behaviors. In addition, brain-derived neurotrophic factor (BDNF) and acetylcholine (ACh) levels in the hippocampus and prefrontal cortex were evaluated.Results: Scopolamine significantly decreased both spatial memory and discrimination index (p0.05). In addition, agomelatine significantly increased BDNF levels in both hippocampus and prefrontal cortex compared to the scopolamine group (p<0.05, p0.05).Conclusion: Taken together, these results demonstrated that agomelatine plays a important role in alleviating scopolamine-induced memory impairment. Therefore, we suggest that agomelatine may be a potential agent in the prevention of cognitive impairment.

Carbonic anhydrases (CAs) are zinc-containing metalloenzymes that catalyze the reversible conversion of carbon dioxide and water into bicarbonate and protons, contributing to acid–base balance, pH regulation, and ion transport. Among human cytosolic isoforms, carbonic anhydrase I (CA I) and carbonic anhydrase II (CA II) are abundant and clinically relevant, yet their distinct roles are often obscured within broader discussions of the CA family. This narrative review evaluates CA I and CA II as biomarkers and therapeutic targets in glaucoma, atherosclerosis and vascular calcification, anemia, epilepsy, Alzheimer’s disease, obstructive sleep apnea, obesity-related metabolic dysfunction, and selected cancers. CA II emerges as the more established pharmacological target, particularly in glaucoma, with acetazolamide and sultiame showing therapeutic potential in obstructive sleep apnea and possible contributions to epilepsy and neurodegeneration through pH regulation, bicarbonate-dependent signaling, and mitochondrial function. CA I instead appears more valuable as a disease-associated biomarker, especially in disorders involving erythrocyte turnover, inflammation, anemia, and malignancy, though circulating CA I may be confounded by hemolysis and altered erythrocyte dynamics. Clinical translation requires isoform-selective modulators, tissue-targeted delivery, standardized biomarker assays, and mechanistic models distinguishing primary CA involvement from secondary disease-related changes.

Green tea (Camellia sinensis) contains bioactive catechins, particularly epigallocatechin-3-gallate (EGCG), but traditional infusions and concentrated green tea extracts differ in EGCG content, dosing pattern, product matrix, systemic exposure, and safety. This structured narrative review evaluates how fasting affects EGCG pharmacokinetics and the relevance of increased systemic exposure to hepatotoxicity. Its distinctive contribution is not a further summary of green tea safety but an explicit appraisal of the evidence chain that is generally assumed to connect the two: each link is assessed separately, and the steps that are demonstrated in humans are separated from those that rest on biological inference. Standardized catechin preparations or purified EGCG taken after an overnight fast produce substantially higher peak plasma concentrations and total systemic exposure than when taken with food, although the two randomized within-subject comparisons that establish this effect were small, differed in dose and formulation, and assessed neither hepatic exposure nor liver injury. Evidence linking high EGCG exposure to prooxidant effects, mitochondrial dysfunction, and hepatocellular injury derives mainly from cellular and animal models at concentrations that exceed reported human peak plasma concentrations by roughly one order of magnitude; in mice, caloric restriction renders otherwise non-hepatotoxic EGCG doses hepatotoxic. In humans these outcomes must be kept apart. High-dose, long-term extract use raises serum aminotransferases in a susceptible minority, a laboratory abnormality demonstrated in controlled trials; hepatic adverse events cluster among catechin-rich bolus preparations rather than brewed beverages; and clinically apparent liver injury, documented in registry cases and associated with HLA-B*35:01, is idiosyncratic rather than dose-determined. Progression from the laboratory abnormality to clinically apparent injury has not been established. Fasting therefore increases systemic EGCG exposure, particularly from concentrated preparations, but has not been established as an independent cause of hepatotoxicity in humans. Treating fasting as an exposure-modifying condition rather than a hepatotoxic factor and nutritional state as a graded variable rather than a single category clarifies which precautions are evidence-based and which research questions remain genuinely open. Safety assessments should consider product type, dose, bolus administration, fed or fasting state, concomitant exposures, and individual susceptibility.

Background: Chemotherapy-related cognitive impairment is a debilitating neurocognitive syndrome with no approved treatment. Doxorubicin induces neuroinflammation, disrupts neurotrophic signaling, and impairs synaptic plasticity. Galantamine, an acetylcholinesterase inhibitor, has anti-inflammatory and neuroprotective properties. This study investigated the dose-dependent effects of galantamine (2.5 and 5 mg/kg) on cognitive behavior, neuroinflammation, the BDNF/TrkB pathway, and synaptic plasticity in a rat model of doxorubicin-induced cognitive impairment. Methods: Female Sprague Dawley rats were divided into control, doxorubicin (4 mg/kg/week, i.p.), doxorubicin + galantamine (2.5 mg/kg/day, oral), and doxorubicin + galantamine (5 mg/kg/day, oral) groups. After four weeks, spatial learning and memory were assessed using the Morris water maze, and recognition memory using the novel object recognition test. Hippocampal IL-1β, IL-10, BDNF, and AChE levels were measured by ELISA. Histopathology was assessed by H&E staining. TrkB expression was evaluated by immunohistochemistry, and PSD-95 and synaptophysin by Western blot. Results: Doxorubicin impaired spatial learning and memory and reduced discrimination index in the NOR test. Galantamine, especially at 5 mg/kg, attenuated these deficits. Doxorubicin increased IL-1β and AChE, while decreasing IL-10 and BDNF. Galantamine at both doses reversed IL-1β and AChE increases and increased BDNF; only the 2.5 mg/kg dose increased IL-10. Doxorubicin-induced neuronal shrinkage and apoptosis were ameliorated by galantamine. Doxorubicin upregulated TrkB, which was normalized by high-dose galantamine. Western blot showed that doxorubicin increased PSD-95 and decreased synaptophysin; galantamine did not alter PSD-95 but reversed the synaptophysin decrease at low dose. Conclusions: Galantamine exerts dose-dependent neuroprotective effects against doxorubicin-induced cognitive impairment by reducing neuroinflammation, modulating BDNF and TrkB levels, and preserving presynaptic plasticity. These findings suggest galantamine as a potential option for preventing chemotherapy-related cognitive impairment.