Plants could be used for multiple medicinal purposes. Moringa oleifera (MO) is considered the most famous plant used for this purpose. The present review aimed to spot the light on the recent medicinal, biochemical, and nutritional applications of MO. The plant contains a huge number of nutrients such as fatty acids, amino acids, proteins, polysaccharides, minerals, and vitamins. It has been used to control glucose, lipids, proteins, minerals, vitamins, hormones, and antioxidants in many animals and human models. Its medicinal applications are also varied and wide; it could be used to control and manage lots of disorders. Extracts and isolated ingredients from the plant open the way for many researchers all over the world to study its biochemical and medicinal impact on many experimental and clinical models. The present review spots the light on the recent medicinal and biochemical significance of MO opening the discussion and demonstrating the strengths and weaknesses in the MO research area. Regardless of the contrary concept, we considered MO a promising plant that could be studied for its medicinal applications on both biochemical and molecular levels. We recommended further research on the molecular effects of MO in healthy and diseased models.

Fatty liver injury is a prevalent condition in most farmed fish, yet the molecular mechanisms underpinning this pathology remain largely elusive. A comprehensive feeding trial spanning eight weeks was conducted to discern the potential of dietary chitosan in mitigating the deleterious effects of a high-fat diet (HFD) while concurrently exploring the underlying mechanism. Growth performance, haemato-biochemical capacity, antioxidant capacity, apoptotic/anti-apoptotic gene expression, inflammatory gene expression, and histopathological changes in the liver, kidney, and intestine were meticulously assessed in Nile tilapia. Six experimental diets were formulated with varying concentrations of chitosan. The first three groups were administered a diet comprising 6% fat with chitosan concentrations of 0%, 5%, and 10% and were designated as F6Ch0, F6Ch5, and F6Ch10, respectively. Conversely, the fourth, fifth, and sixth groups were fed a diet containing 12% fat with chitosan concentrations of 0%, 5%, and 10%, respectively, for 60 days and were termed F12Ch0, F12Ch5, and F12Ch10. The results showed that fish fed an HFD demonstrated enhanced growth rates and a significant accumulation of fat in the perivisceral tissue, accompanied by markedly elevated serum hepatic injury biomarkers and serum lipid levels, along with upregulation of pro-apoptotic and inflammatory markers. In stark contrast, the expression levels of nrf2, sod, gpx, and bcl-2 were notably decreased when compared with the control normal fat group. These observations were accompanied by marked diffuse hepatic steatosis, diffuse tubular damage, and shortened intestinal villi. Intriguingly, chitosan supplementation effectively mitigated the aforementioned findings and alleviated intestinal injury by upregulating the expression of tight junction-related genes. It could be concluded that dietary chitosan alleviates the adverse impacts of an HFD on the liver, kidney, and intestine by modulating the impaired antioxidant defense system, inflammation, and apoptosis through the variation in nrf2 and cox2 signaling pathways.

Endothelial dysfunction is considered one of the main causes of atherosclerosis and elevated blood pressure. Atherosclerosis (AS) formation is enhanced by different mechanisms including cytokine generation, vascular smooth muscle cell proliferation, and migration. One of the recent treatment toward endothelial dysfunction is vinpocetine (VPN). VPN is an ethyl apovincaminate used in the management of different cerebrovascular disorders and endothelial dysfunction through inhibition of atherosclerosis formation. VPN is a potent inhibitor of phosphodiesterase enzyme 1 (PDE1) as well it has anti-inflammatory and antioxidant effects through inhibition of the expression of nuclear factor kappa B (NF-κB). VPN has been shown to be effective against development and progression of AS. However, the underlying molecular mechanism was not fully clarified. Consequently, objective of the present narrative review was to clarify the mechanistic role of VPN in AS. Most of pro-inflammatory cytokines released from macrophages are inhibited by the action of VPN via NF-κB-dependent mechanism. VPN blocks monocyte adhesion and migration by inhibiting the expression of pro-inflammatory cytokines. As well, VPN is effective in reducing oxidative stress, a cornerstone in the pathogenesis of AS, through inhibition of NF-κB and PDE1. VPN promotes plaque stability and prevent erosion and rupture of atherosclerotic plaque. In conclusion, VPN through mitigation of inflammatory and oxidative stress with plaque stability effects could be effective agent in the management of endothelial dysfunction through inhibition of atherosclerosis mediators.

Acute Myeloid Leukemia (LAML) is a life-threatening hematological malignancy, and the DEAD-box helicase 3 X-linked (DDX3X) gene is a potential yet underexplored target gene for LAML. Biomolecules derived from medicinal plants like Aerva javanica offer a great source of therapeutic candidates. This study aimed to investigate the role of DDX3X in LAML and identify plant-derived biomolecules that could inhibit DDX3X using computational approaches. Pan-cancer mutational profiling, a transcriptomic analysis, survival, protein–protein interaction networks, and a principal component analysis (PCA) were employed to elucidate functional associations and transcriptomic divergence. Subsequently, biomolecules from A. javanica were subjected to in silico screening using molecular docking and ADMET profiling. The docking protocol was validated using RK-33, a known DDX3X inhibitor. DDX3X was found to be linked to key leukemogenic pathways, including Wnt/β-catenin and MAPK signaling, indicating it to be a potential target. Molecular docking of A. javanica compounds revealed CIDs 15559724, 5490003, and 74819331 as potent DDX3X inhibitors with strong binding affinity and favorable pharmacokinetic and toxicity profiles compared to RK-33. This study highlights the importance of DDX3X in LAML pathogenesis and suggests targeting it using plant-derived inhibitors, which may require further in vitro and in vivo validation.