The aim of this study is to investigate the effect of propolis, which may have estrogenic effects, on myocardial ischemia/reperfusion (mI/R) injury not only in male rats but also in intact and ovariectomized (ovx) female rats. Six groups were formed: untreated males (n = 8), treated males (n = 9), untreated intact females (n = 9), treated intact females (n = 10), untreated ovx females (n = 10), and treated ovx females (n = 8). An alcoholic extract of a single dose of propolis (200 mg/kg) was administered orally daily for 14 days. Thirty minutes of ischemia and 120 min of reperfusion were performed. Blood pressure, heart rate, arrhythmias (ventricular premature contraction [VPC], ventricular tachycardia [VT], ventricular fibrillation [VF]), and myocardial infarct size were evaluated. Total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and 17 beta-estradiol (E2) were measured. The untreated females showed more resistance to mI/R injury than the untreated males, as evidenced by lower duration, incidence, and score of arrhythmias, and smaller infarct size (p < .05). After ovx, this resistance disappeared. Propolis improved these values in treated males and treated ovx females (p < .05). Propolis increased TAS in treated males and decreased TOS in treated ovx females as well as elevated SOD in all treated groups (p < .05). Propolis decreased E2 level in treated intact females; however, it increased E2 level in treated ovx females (p < .05). The results revealed that propolis could protect the heart against mI/R injury in males and ovx females. Practical applications It is known that the female heart has an increased sensitivity to myocardial ischemia/reperfusion (mI/R) injury due to estrogen deficiency and/or estrogen deprivation following menopause or surgical removal of the ovaries. Propolis has the potential to mimic estrogen under physiological and pathophysiological conditions, as well as its antioxidant property. The results indicated that propolis decreased myocardial infarct size, arrhythmia score, arrhythmia duration, and incidence in ovariectomized female rats and male rats. In addition, the present results demonstrated that an alcoholic extract of propolis as a natural product can effectively maintain the resistance of female heart to mI/R injury after estrogen deficiency.

Exposure to cigarette smoke leads to an increase in oxidative stress within the body, resulting in both an elevated oxidant burden and a compromised antioxidant defense system. This imbalance creates a significant risk factor for various diseases by promoting cellular damage, inflammation, and toxicity. The oxidants present in cigarette smoke are considered the primary contributors to these pathological conditions. Supporting the antioxidant system with specific bioactive compounds may help mitigate the toxic effects caused by cigarette smoke. In this study, the effects of EGCG pre‐administration on the antioxidant system were evaluated under both acute and chronic exposure conditions to cigarette smoke. Different doses of EGCG were administered to determine its potential role in oxidative stress regulation, and histopathological examinations and antioxidant enzyme levels were assessed. The findings demonstrated that while acute EGCG administration did not significantly improve antioxidant enzyme activity, chronic administration of EGCG at a dose of 50 mg/kg effectively increased antioxidant enzyme production, reduced oxidative stress, and liver injury. In the presence of cigarette smoke, EGCG contributed to the stabilization of oxidative stress markers. However, chronic EGCG administration in the absence of oxidative stressors requires further investigation to assess its impact on other organs. EGCG appears to be a promising candidate for alleviating the adverse effects of external oxidant exposure and mitigating oxidative stress. However, its long‐term application and potential side effects in different physiological conditions should be explored further examinations. Although acute EGCG application did not enhance antioxidant enzyme levels, it unexpectedly elevated oxidative stress, emphasizing the need for more comprehensive studies to clarify its mechanisms and optimize its usage. We further identify the principal underlying mechanisms involved in this process.

Objective: This study aims to contribute novel insights by investigating the potential positive effects of a combined dietary supplement and exercise program on mitochondrial oxidative stress and energy metabolism in aging. Focusing on the protective impact of Alpha Lipoic Acid (ALA), a potent antioxidant, against exercise-induced mitochondrial oxidative stress in rats, we also assess how L-Carnitine administration affects exercise ability by analyzing resistin and HbA1c levels, indicators linked to insulin resistance and cellular sensitivity. Methods: In this 10-day study, 42 old male Sprague Dawley rats (weighing 400±10 g, aged 15–17 weeks) were divided into six groups (n=7): Control, Exercise, L-Carnitine, Alpha Lipoic Acid (ALA), L-Carnitine+Exercise, ALA+Exercise. Relevant groups received daily oral gavage doses of L- Carnitine (50 mg/ml) and ALA (18 mg/ml). Exercise groups underwent treadmill sessions. On day 10, blood samples were quantitatively analyzed for HbA1c and Resistin levels using a Cusabio ELISA assay kit (China). Results: ALA supplementation synergistically reduced resistin and HbA1c levels, individually and combined with exercise. Conversely, L-Carnitine supplement, alone or with exercise, increased resistin levels but it caused a decrease in HbA1c levels. Conclusions: The data indicated a minor, insignificant decrease in resistin levels for the exercise and ALA groups, with a statistically significant difference in HbA1c levels among all groups. Exercise alone positively impacted both HbA1c and resistin levels, suggesting a potential counteraction of age-related oxidative stress and a positive influence on energy metabolism through an appropriate diet and exercise program. Further studies are required to explore specific metabolic pathways and relationships identified in our findings.