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Background Cancer chemotherapy is difficult because current medications for the treatment of cancer have been linked to a slew of side effects; as a result, researchers are tasked with developing greener cancer chemotherapies. Moringa oleifera has been reported with several bioactive compounds which confirm its application for various ailments by traditional practitioners. In this study, we aim to prospect the therapeutic potentials of M. oleifera phytocompounds against cancer proliferation as a step towards drug discovery using a computational approach. Target proteins: dihydrofolate reductase (DHFR) and B-Cell Lymphoid-2 (BCL-2), were retrieved from the RCSB PDB web server. Sixteen and five phytocompounds previously reported in M. oleifera leaves (ML) and seeds (MS), respectively, by gas chromatography–mass spectrometry were synthesized and used in the molecular docking study. For accurate prediction of binding sites of the target proteins; standard inhibitors, Methotrexate (MTX) for DHFR, and Venetoclax (VTC) for BCL-2, were docked together with the test compounds. We further predicted the ADMET profile of the potential inhibitors for an insight into their chance of success as candidates in drug discovery. Results Results for the binding affinities, docking poses, and the interactions showed that ML2, ML4-6, ML8-15, and MS1-5 are potential inhibitors of DHFR and BCL-2, respectively. In the ADMET profile, ML2 and ML4 showed the best drug-likeness by non-violation of Lipski Rule of Five. ML4-6, ML8, ML11, ML14-15, and MS1, MS3-5 exhibit high GI absorption; ML2, ML4-6, ML8, MS1, and MS5 are blood–brain barrier permeants. ML2, ML4, ML9, ML13, and MS2 do not interfere with any of the CYP450 isoforms. The toxicity profile showed that all the potential inhibitors are non-carcinogenic and non-hERG I (human ether-a-go-go related gene I) inhibitors. ML4, ML11, and MS4 are hepatotoxic and ML7, ML10, and MS4 are hERG II inhibitors. A plethora of insights on the toxic endpoints and lethal concentration values showed that ML5, ML13, and MS2 are comparatively less lethal than other potential inhibitors. Conclusion This study has demonstrated that M. oleifera phytocompounds are potential inhibitors of the disease proteins involved in cancer proliferation, thus, an invaluable step toward the discovery of cancer chemotherapy with lesser limitations.

This study demonstrated the therapeutic potentials of Cucumeropsis mannii seed oil (CMSO) capable of alleviating BPA‐induced dyslipidemia and adipokine dysfunction. In this study, we evaluated the effects of CMSO on adipokine dysfunctions and dyslipidemia in bisphenol‐A (BPA)‐induced male Wistar rats. Six‐week‐old 36 albino rats of 100–200 g weight were assigned randomly to six groups, which received varied doses of BPA and/or CMSO. The administration of BPA and CMSO was done at the same time for 42 days by oral intubation. The adipokine levels and lipid profile were measured in adipose tissue and plasma using standard methods. BPA induced significant (p < .05) increases in triglycerides, cholesterol, leptin, LDL‐C, and atherogenic and coronary risk indices in adipose tissue and plasma, as well as a decrease in adiponectin and HDL‐C levels in Group II animals. BPA administration significantly (p < .05) elevated Leptin levels and reduced adiponectin levels. BPA plus CMSO reduced triglycerides, cholesterol, leptin, LDL‐C, and atherogenic and coronary risk indices while increasing adiponectin levels and HDL‐C in adipose tissue and plasma (p < .05). The results showed that BPA exposure increased adipose tissue as well as serum levels of the atherogenic index, triglycerides, cholesterol, coronary risk index, LDL‐C, leptin, and body weight with decreased adiponectin levels and HDL‐C. Treatment with CMSO reduced the toxicities caused by BPA in rats by modulating the body weight, adiponectin/leptin levels, and lipid profiles in serum and adipose tissue. This study has shown that CMSO ameliorates BPA‐induced dyslipidemia and adipokine dysfunctions. We suggest for further clinical trial to establish the clinical applications.

There has been increasing search for the ameliorative properties of seed oils against toxicants. bisphenol A acts as an estrogenic endocrine‐disrupting chemical capable of causing male infertility. This study aimed to explore Cucumeropsis mannii seed oil effects against mitochondrial damage in rats using bisphenol A. Forty‐eight rats were randomly assigned to six groups (n = 6) of eight rats each and fed the same food and water for 6 weeks. The group A rats were given 1 mL olive oil, while the ones in group B were given bisphenol A at 100 mL/kg body weight via oral route. Group C received C. mannii seed oil 7.5 mL/kg body weight C. mannii seed oil, while group D, group E, and group F were pre‐administered bisphenol A at 100 mL/kg body weight, followed by treatment with C. mannii seed oil at 7.5, 5, and 2.5 mL/kg body weight, respectively. Antioxidant enzymes, glutathione, reactive oxygen species, testicular volume, malondialdehyde, body weight, and testicular studies were done using standard methods. The results of the bisphenol A‐administered group showed a significant decrease in the antioxidant enzymes, glutathione, body weight, and testicular volume with elevation in the levels of reactive oxygen species, malondialdehyde, and testicular indices. BPA + CMSO‐treated group showed a significant increase in GPx activity compared with BPA‐exposed rats. CMSO treatment significantly increased catalase activity in comparison with that of rats exposed to BPA. Remarkably, C. mannii seed oil and bisphenol A co‐administration significantly reversed the abnormalities observed in the dysregulated biochemical biomarkers. Our findings suggest that C. mannii seed oil has considerable antioxidant potential which can be explored in therapeutic development against systemic toxicity induced by exposure to bisphenol A. Cucumeropsis mannii seed oil protects against bisphenol A‐induced testicular mitochondria damages.

Background: The world is currently battling with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that originated in Wuhan, China late December 2019 and has now become a global pandemic. Objective: From the available scientific evidence, attempt was made to elucidate the possible molecular basis that underlays the severity of this disease with the aim of unveiling a novel therapeutic target for the development of effective therapy against this menace. Methods: Systematic MEDLINE (Ovid) and other databases such as EMBASE were searched for published articles up to June 2020. The subject heading/keywords – “novel coronavirus”, “2019 novel coronavirus”, “2019-nCoV”, “COVID-19”, “SARS-CoV-2 and Cytokines” were used. Results: The investigation revealed that SARS-CoV-2 having distinct tropism of nasal mucosa, negotiates its way into the host’s cells prominently through type II pneumocytes of the lungs using its SPIKE (S protein) recognition binding domain (RBD) on the host’s angiotensin-converting enzyme 2 (ACE2) receptors. Inside the cells, they rapidly replicate, avoiding the type I interferons (IFN-1) signaling crucial to the initial viral control. The delayed IFN-1 marshaling results to the encroachment of the neutrophils, mononuclear macrophages as well as cytokines/chemokines to the site of infections well above the threshold resulting in conditions known as hyper-cytokineamia (cytokine storm). This socalled “cytokine storm” orchestrates and exacerbates systemic hyper-inflammation, which induces lung injury and subsequently acute respiratory distress syndrome (ARDS), multiple system organ failure (MSOF) and eventual death of the patients. Conclusions: Modulating the expression and exacerbation of cytokines such as IL-6 and IL-1β may be a novel therapeutic approach against late stage COVID-19.