Introduction. Moringa leaves (Moringa oleifera), which are members of the Moringaceae family, are one of the herbal plants that are widely known in Indonesia. Phytochemical contents of moringa leaf, such as flavonoid, quercetin, and phenolic acid, are believed to have an effect on improvement of NAFLD. Therefore, moringa leaf is considered as one the herbal plants that can be used as supplementation in the form of adjuvant therapy to NAFLD. The study objective of our research is to review the effect of giving moringa leaf to the liver, especially the histopathologic features. This study will be conducted on literature review research design, more specifically in the form of a systematic review. Research Method. Five major electronic web databases, including PubMed, Cochrane Library, Google Scholar, Scopus, and ScienceDirect, were used in identifying literature from 2014 to 2023. Results. From a comprehensive analysis of 13 relevant literature sources, we elucidate the impact of Moringa oleifera leaf extract on liver histopathology, glucose, and lipid metabolism. Furthermore, we provide insights into its safety profile concerning human health. Conclusion. The phytochemical content of Moringa oleifera leaf extract had shown a significant benefit in plant medicinal sector. From the research that had been done, Moringa oleifera leaf extract contributes to give significant improvement on liver histopathological features, glucose, and lipid metabolism on animal sample model.

The immediate early gene exhibits activation markers in the nervous system consisting of ARC, EGR-1, and c-Fos and is related to synaptic plasticity, especially in the hippocampus. Immediate early gene expression is affected by physical exercise, which induces direct ARC, EGR-1, and c-Fos expression. Objective: To assess the impact of exercise, we conducted a literature study to determine the expression levels of immediate early genes (ARC, c-Fos, and EGR-1). Methods: The databases accessed for online literature included PubMed-Medline, Scopus, and ScienceDirect. The original English articles were selected using the following keywords in the title: (Exercise OR physical activity) AND (c-Fos) AND (Hippocampus), (Exercise OR physical activity) AND (ARC) AND (Hippocampus), (Exercise OR physical activity) AND (EGR-1 OR zif268) AND (Hippocampus). Results: Physical exercise can affect the expression of EGR-1, c-Fos, and ARC in the hippocampus, an important part of the brain involved in learning and memory. High-intensity physical exercise can increase c-Fos expression, indicating neural activation. Furthermore, the expression of the ARC gene also increases due to physical exercise. ARC is a gene that plays a role in synaptic plasticity and regulation of learning and memory, changes in synaptic structure and increased synaptic connections, while EGR-1 also plays a role in synaptic plasticity, a genetic change that affects learning and memory. Overall, exercise or regular physical exercise can increase the expression of ARC, c-Fos, and EGR-1 in the hippocampus. This reflects the changes in neuroplasticity and synaptic plasticity that occur in response to physical activity. These changes can improve cognitive function, learning, and memory. Conclusion: c-Fos, EGR-1, and ARC expression increases in hippocampal neurons after exercise, enhancing synaptic plasticity and neurogenesis associated with learning and memory.

The mechanism for cardiac hypertrophy process that would be a benefit for improvement of cardiovascular endurance needed to be investigated throughly. Specific intensity of training may play a role for homeostasis process in cardiac during training. In the present study, we examine the effect of different intensity of treadmill training on cardiac hypertrophy process and autophagy related gene expression in male wistar rats. Three different intensities of treadmill training were conducted on 15 male wistar rats (Low Intensity: 10 m/minute, Moderate Intensity: 20 m/minute, and High Intensity: 30 m/minute) compared to 5 sedentary rats as control. Training duration was 30 min per day, frequency was 5 days per week, during 8 weeks period. Heart weight and heart weight/body weight ratio were measured after the experiments. Left ventricle myocardium was taken for microscopic analysis with HE staining. mRNA was extracted from left ventricle myocardium for examining αMHC and autophagy related gene expression (PIK3CA, mTOR, LC3, p62) using semi quantitative PCR. We observed that altered training intensity might stimulate cardiac hypertrophy process. MI and HI training increased heart weight and heart weight/body weight ratio. This finding is supported by microscopic result in which cardiac hypertrophy was found in MI and HI, with focal fibrosis in HI, and increased αMHC gene expression in MI (p < 0.05) and HI (p = 0.076). We also observed decreased PIK3CA (LI 0.8 fold, MI 0.9 fold), mTOR (LI 0.9 fold, MI 0.9 fold), LC3 (LI 0.9 fold, MI 0.8 fold, HI 0.8 fold), and p62 (LI 0.8 fold, MI 0.9 fold) compared to control. Interestingly, we found increased mTOR (HI 1.1 fold) and p62 (HI 1.1 fold) compared to control. Training with different intensity creates different cardiac hypertrophy process based on heart weight and heart weight/body weight ratio, microscopic examination and autophagy related gene expression.

Aerobic training has a beneficial effect on enhancing liver functions. Autophagy might potentially play a role in preventing excessive lipid accumulation, regulating oxidative stress, and inflammation in the liver. To investigate the potential linking role of autophagy-related gene expressions and protein levels with histopathology changes in Wistar rat livers after treadmill training under different intensities. 20 rats were divided into 4 groups (control, low intensity, moderate intensity, and high intensity). 8 weeks of treadmill training was conducted with a frequency of 5 days per week, for a duration of 30 min per day. Liver histopathology was studied using hematoxylin-eosin, and oil red O staining. RNA and protein from the liver tissues were extracted to examine the autophagy-related gene (LC3, p62) and protein levels (Beclin, ATG5, LC3, p62). The gene expressions of CPT1a, CD36, FATP 2,3,5, GLUT2, and FGF21 were also studied. Different intensities of training might potentially modulate autophagy-related gene expressions in rat livers. LC3 and p62 mRNA expressions in moderate and high intensities decreased compared to control. Beclin, ATG5, and LC3 protein level increased compared to control, while p62 protein level decreased compared to control. Whereas for the other genes, we found an increase in CPT1a, but we did not observed any changes in the expression of the other genes. Interestingly, autophagy-related gene expressions might be correlated with the changes of sinusoidal dilatation, cloudy swelling, inflammation, and lipid droplets of the liver tissues. Moderate and high intensities of training induce autophagy activity, combined with a shift in metabolic zonation in liver that might be potentially correlated with lipophagy. Our results showed the potential interplay role between autophagy and liver histopathology appearances as a part of the adaptation process to training.

The popularity of the electronic cigarette has soared in the last decades. However, the health effect of smoking electronic cigarettes on the vascular system is unclear. This systematic review examines the electronic cigarettes effect on the vascular system from recent evidence. A systematic search was conducted in MEDLINE (PubMed) database from January 2016 to August 2021 for studies assessing the vascular effect of chronic use of electronic cigarettes on human and animal. The Cochrane Risk of Bias 2, NIH Quality Assessment for Cross-Sectional Study, and SYRCLEs Risk of Bias were used to assess the risk of bias in interventional, observational, and animal study, respectively. A narrative synthesis of evidence is provided to describe results. From 101 retrieved studies related to electronic cigarettes effect on the vascular system, a total of 16 studies are included in this review. The overall results indicated that electronic cigarette use is associated with adverse events in the vascular, including the incident of elevated oxidative stress, endothelial dysfunction, inflammation, arterial stiffness, and the development of atherosclerotic lesion. Further studies should broaden perspectives and reveal more about the mechanism of how electronic cigarettes impact on vascular system.