Propolis as an autophagy modulator in relation to its roles in redox balance and inflammation regulation.

Autophagy is a degradation process that is evolutionarily conserved and is essential in maintaining cellular and physiological homeostasis through lysosomal removal and elimination of damaged peptides, proteins and cellular organelles. The dysregulation of autophagy is implicated in various diseases and disorders, including cancers, infection-related, and metabolic syndrome-related diseases. Propolis has been demonstrated in various studies including many human clinical trials to have antimicrobial, antioxidant, anti-inflammatory, immune-modulator, neuro-protective, and anti-cancer. Nevertheless, the autophagy modulation properties of propolis have not been extensively studied and explored. The role of propolis and its bioactive compounds in modulating cellular autophagy is possibly due to their dual role in redox balance and inflammation. The present review attempts to discuss the activities of propolis as an autophagy modulator in biological models in relation to various diseases/disorders which has implications in the development of propolis-based nutraceuticals, functional foods, and complementary therapies.

Comparison impact of cigarettes and e-cigs as lung cancer risk inductor: a narrative review.

Smoking cigarettes contributes to lung cancer progression and the development of other respiratory diseases. E-cigs are increasingly being offered to mitigate the harmful effects of traditional cigarettes and eventually for smoke cessation. Because e-cigs do not burn tobacco, it stands to reason that vaping e-liquid is less harmful than inhaling cigarette smoke. This study critically assessed the underlying biological effects of cigarettes and e-Cigs. We searched PubMed databases to elucidate the fundamental, potentially carcinogenic, molecular pathways and the possible effects of cigarettes and e-cigs products on lung cancer progression. Cigarette smoke leads to chronic obstructive pulmonary disease (COPD), while e-cigs have contributed to lung injury. Cigarette smoke and e-cigs increase proinflammatory cytokine expression in cells and affect protein regulation, leading to an increased lung cancer risk. E-cigs are quickly gaining popularity among consumers. Vaping-related diseases and deaths have attracted attention on a global scale. Excessive nicotine levels in e-liquid have the potential to cause severe toxicity, which can lead to neurological and brain damage and respiratory failure, as well as death. Thus, the toxic effects of e-cigs aerosol exposure are essentially identical to that caused by combustible cigarette smoking.

Effect of different intensities aerobic exercise to cardiac angiogenesis regulation on Wistar rats.

The adaptation response of myocardium angiogenesis stimulated by specific exercise intensities remains unclear. The aims of this study is to explore the effect of different intensities aerobic exercise to cardiac angiogenesis regulation via HIF-1α, PGC-1α, VEGF, and CD34+ in Wistar rats. Wistar rats were divided into control and exercise groups. Exercise groups were trained on a treadmill for 12 weeks, 30 min/day for 5 days with low, moderate, and high-intensity groups. The rats were sacrificed, and the myocardium was collected and preserved at -80°C until used. Cardiac protein samples were extracted and run for Western blotting using the specific antibodies: hypoxia-inducible factor (HIF)-1α, Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), vascular endothelial growth factor (VEGF), and Cluster of differentiation 34 (CD34+). Results showed that protein expression of HIF-1α, PGC-1α, VEGF, and CD34+ was increased significantly by different intensities in the exercise group compared to the control. A correlation statistics test showed that there was a strong correlation effect of HIF-1α on VEGF protein expression in low (p=0.047) and high intensity exercise groups (p=0.009), but no effect was found in the moderate groups. In addition, there was a significant strong effect of PGC-1α on VEGF protein expression in the moderate groups (p=0.037), but no effect was found in other groups. In conclusion, different exercise intensities induce a different modulation pattern of proteins which might be responsible for cardiac adaptation, especially angiogenesis.

Moringa oleifera Leaves Extract Alters Exercise-Induced Cardiac Hypertrophy Adaptation.

<b>Background and Objective:</b> Cardiomyocyte adaptation to exercise might require ROS as a central regulator. There is a limited study regarding the importance of ROS for inducing exercise-induced adaptation and its correlations with changes in histological scoring of cardiac muscles. The study aimed to explore the importance of physiological ROS induced by exercise and its correlation with Cardiomyocyte' histological appearance that is altered by <i>Moringa oleifera</i> leaves extract in Wistar rats. <b>Materials and Methods:</b> This was an animal experimental study, which use 4 groups of 24 Wistar rats divided into Control (Co), <i>Moringa</i> leaves extract (Mo), Exercise (Ex) and a combination of <i>Moringa </i>leaves extract and Exercise (MoEx). The <i>Moringa</i> leaves extract were given orally, 5 days a week, for 4 consecutive weeks. The exercise was given in moderate intensity, 5 days a week, also for 4 consecutive weeks. <b>Results:</b> This study found significant differences in heart weight and heart weight/body weight ratio in Ex group compared to the control. As for histology scoring, found that MoEx group has 16.7% cardiac hypertrophy and myofiber disarray compared to 83.3% mild hypertrophy and 50% mild disarray in Ex group. <b>Conclusion:</b> In summary, the study showed that the potential central role of exercise-induced physiological ROS for cardiac hypertrophy adaptation is altered by <i>Moringa oleifera </i>leaves extract treatment.