Kayode Komolafe

Vernonia calvoana (VC), a commonly used medicinal plant in West Africa, has been shown by our research team to inhibit the proliferation of OVCAR-3 ovarian cancer cells through mechanisms involving oxidative stress, DNA damage, and S-phase cell cycle arrest. The objective of the current study was to elucidate the intrinsic apoptotic mechanisms triggered by VC fraction seven (VCF7). OVCAR-3 cells were treated with VCF7 (0, 8, 16, and 32 μg/mL) for a duration of 48 h. Apoptosis was assessed using Annexin V/Propidium Iodide (PI) staining followed by flow cytometry analysis. Mitochondrial membrane potential (ΔΨm) was assessed through JC-1 staining and confocal microscopy, while chromatin condensation was analyzed using DAPI staining. DNA fragmentation was examined by agarose gel electrophoresis. Caspase 3 activity was measured using flow cytometry. Protein expression levels of p53, Bcl-2, cytochrome c, caspase-9, and caspase-3 were determined by Western blot analysis, and mRNA expression levels of p53 and Bcl-2 were evaluated using qRT-PCR. VCF7 induced apoptosis in a concentration-dependent manner. Analysis using Annexin V/PI indicated an increase in apoptotic cell populations from 10.5% to 30%, along with a rise in necrotic cells from 7% to 50% across treatment concentrations. A modest, concentration-associated decrease in mitochondrial membrane potential was recorded (0.96-, 0.88-, and 0.85-fold at 8, 16, and 32 μg/mL, respectively; p < 0.05). DAPI staining validated the concentration-dependent chromatin condensation and nuclear fragmentation. The analysis of DNA fragmentation showed progressive internucleosomal degradation, appearing as a smear pattern with distinct fragments at elevated concentrations, indicative of concurrent apoptotic and necrotic cell death. The activation of caspase-3 reached a peak of 28% at 16 μg/mL. Western blot analysis indicated an upregulation of p53, a downregulation of Bcl-2, an increase in total cytochrome c protein levels, and an increased expression of caspase-9 and caspase-3 in a concentration-dependent manner. These findings were corroborated at the transcriptional level by qRT-PCR, which showed increased p53 mRNA and decreased Bcl-2 mRNA expression. Taken together, these results underscore the potential of VCF7 as a promising plant-derived anticancer agent and support the need for further preclinical and clinical studies in ovarian cancer.

Peptic ulcer is a multifactorial and debilitating gastrointestinal disorder affecting about 10 million people worldwide. The effectiveness of many anti-ulcer drugs is often limited by adverse effects, thereby making the need for safer, natural alternatives necessary. In this study, experimental rats were orally gavaged for 14 days with 1.25, 2.5, or 5.5 mg/kg body weight of lyophilized goat weed (Ageratum conyzoides) juice extract (ACJE). Gastric ulceration was induced in fasted animals by oral administration of ethanol (96%, 5 mL/kg). Animals were subsequently euthanized to evaluate the ulcer index, stomach histology, and biochemical markers of toxicity and oxidative stress. Untreated, induced rats had significantly (p < 0.001) higher ulcer scores (9-fold) and gastric juice secretion (1.5-fold), as well as lower gastric juice pH (1.5-fold). These effects were markedly reversed by ACJE pretreatment. Rats administered 2.5 mg/kg ACJE demonstrated similar protective benefits to those of ranitidine, including significant reductions in ulcer severity, gastric juice volume, and acidity. Furthermore, ulcer-associated dyslipidemia and changes in LDL and HDL cholesterol levels were mitigated in ACJE-pretreated animals. The gastroprotective effect of ACJE was validated by histological findings and the restoration of oxidative stress in rats. In silico analysis revealed that ACJE phytochemicals bind strongly to urease and pepsin, with higher docking scores compared to standard drugs. Overall, ACJE shows promising gastroprotective potential, necessitating more mechanistic research.

Plant‐derived foods are rich in bioactive compounds with notable therapeutic potential. Plantain ( Musa paradisiaca L.) is widely cultivated and traditionally used in managing inflammation and diabetes. This study investigated the cardioprotective effects of the ethanol extract of a polyphenol‐rich unripe (green) M. paradisiaca peel in a rat model of type 2 diabetes. Bioactive compounds were identified using GC‐FID, followed by molecular docking with relevant protein targets. Type 2 diabetes was induced using a high‐fat diet (12 weeks) and streptozotocin (35 mg/kg). Diabetic rats were treated with 200 and 400 mg/kg extract for 30 days. HFD/STZ‐induced diabetic rats showed elevated fasting blood and serum glucose, dyslipidemia, increased creatine kinase‐MB, lactate dehydrogenase, interleukin‐6, C‐reactive protein, tumor necrosis factor‐α, and troponin I, all significantly reduced by the extract. Reduced adiponectin levels were significantly improved ( p < 0.05), alongside the attenuation of oxidative stress. Histology revealed reduced myocyte degeneration and inflammatory cell infiltration with evidence of regeneration. Molecular docking suggested that polyphenols contributed to the observed antidiabetic activity. In conclusion, the ethanol extract of green plantain peels possesses antihyperglycemic, antidyslipidemic, anti‐inflammatory, antioxidant, and cardioprotective properties.

Plantain (Musa paradisiaca L.) is a tropical monocotyledonous, succulent plant of the Musaceae family commonly grown for food in the tropical regions of the African, Asian, and South American continents, where its parts are also sought for ethnomedicinal purposes in the treatment of burns, inflammation, and diabetes, among others. In the present preliminary exploratory study, the ethanol extract of the underutilized Musa paradisiaca peel (MPE) was evaluated for its in vitro inhibitory effects on α-amylase and α-glucosidase, as well as its in vivo hypoglycemic activity and potential biochemical toxicity. MPE (100, 200, 400 mg/kg) was orally administered to normal experimental rats for 30 days, following which the lipid profile, antioxidant status, and serum/tissue indices of hepatic, renal, and cardiac functions were evaluated. MPE produced significant inhibition (p < 0.05) of α-amylase (37%) and α-glucosidase (46%) at 120 µg/mL in vitro. The effect was lower than that of acarbose (IC₅₀ = 44.4 ± 1.14 and 15.60 ± 0.01 µg/mL, respectively). A modest blood glucose-lowering effect of MPE was observed at the highest tested dose (400 mg/kg) following subacute oral administration. During this treatment period, no biochemical alterations of toxicological importance were caused by MPE, as the organ–body weight ratio and serum/tissue indicators of organ function/damage were not adversely altered. In conclusion, MPE demonstrated inhibitory activity against both α-amylase and α-glucosidase, which may contribute to its potential hypoglycemic effects. Additionally, the findings indicate that the peel extract is non-toxic in rats following sub-acute administration at doses up to 400 mg/kg body weight. Further studies involving diabetic models and chronic exposure will substantiate and extend these preliminary observations.

Gastroesophageal reflux disease (GERD) is a common gastrointestinal disorder that is defined by the reflux of gastric contents into the esophagus, and it results in symptoms such as esophageal inflammation, regurgitation, and indigestion. Although proton pump inhibitors (PPIs) and histamine-2 receptor antagonists are frequently employed to treat GERD, their prolonged administration is associated with adverse effects, necessitating the development of alternative therapeutic strategies. Natural products are now recognized as promising candidates for the management of GERD due to their bioactive compounds, which possess antioxidant, anti-inflammatory, and mucosal-protective properties. The potential of natural products in the treatment of GERD is comprehensively examined in this review, with a focus on their mechanisms of action, which include acid suppression, esophageal mucosal regeneration, anti-inflammatory activity, and gut microbiota modulation. Also, the efficacy and safety of key natural products, including flavonoids, polyphenols, plant-derived oils, herbal extracts, probiotics, and dietary components, in preclinical and clinical studies, are assessed. Additionally, this review addresses the barriers confronting the translation of natural therapies into clinical practice, such as regulatory obstacles, variability in bioavailability, and the need for dosage standardization. The integration of natural products into the management of GERD has the potential to enhance conventional therapies, providing a more comprehensive and secure approach for patients.

The neem plant (Azadirachta indica) has popular ethnomedicinal applications. The anti-diabetic potential and mechanism of neem seed oil (NSO) in a rodent model of type 2 diabetes mellitus was evaluated in the present study. Experimentally-induced diabetic animals were administered NSO (200 and 400 mg/kg) or metformin (150 mg/kg) orally for 30 days, with some animals serving as positive and negative controls. NSO significantly (p < .05) reversed diabetes-induced impaired glucose metabolism, dyslipidaemia, and oxido-inflammatory imbalances typified by changes in the NADH/NAD+ ratio (p < .001) and increases in the mRNA or protein levels of C-reactive protein, 4-hydroxynonenal, and pro-inflammatory cytokines (TNF-α and Il-1β) among others in the hepatic or pancreatic tissues of diabetic animals. The histological evaluation of the pancreatic tissue corroborated the protective effect of NSO. The findings showed that the antidiabetic effect of NSO proceeded through its hypolipidemic effect and modulation of redox and inflammatory signalling events in the tissues of animals.

For a long time, traditional medicine has relied on the use of medicinal plants and herbal products which have served as the basis for numerous pharmaceuticals. Parkia biglobosa (Jacq) R.Br.ex. G. Don., commonly called the African locust bean tree, is a perennial deciduous plant native to West Africa where it is highly esteemed for its nutritional and traditional medicinal benefits. Parkia biglobosa’s ethnomedicinal uses include microbial infections such as diarrhea and chronic diseases like hypertension and type 2 diabetes mellitus. This article presents the current understanding of the molecular mechanisms underlying Parkia biglobosa’s biological effects. An electronic database search was conducted using P. biglobosa and its synonyms as keywords in Scientific Electronic Library Online, ISI Web of Knowledge, PubMed, Scopus, Science Direct, and Google Scholar. Consistently, scientific research has confirmed the medicinal effects of the plant’s extracts and active phytochemicals, including antimicrobial, analgesic, antidiabetic, antihypertensive, hypolipidemic, and neuroprotective properties, among others. It highlights the contributions of identified innate phytochemicals and existing limitations to therapeutic applications, as well as the need for and prospects for further research. Advancing our understanding of the medicinal plant’s biological mechanisms and the contributions of the active phytochemicals would allow for more effective exploration of its vast pharmacological potential and facilitate clinical applications.

Neem (Azadirachta indica) plant components are popularly applied in ethnomedicine for the management of numerous diseases. The current study aimed to assess the anti-diabetic potential and mechanism of neem seed oil (NSO) in a rodent model of type 2 diabetes mellitus induced by a chronic high-fat diet and a single low-dose of streptozotocin. Diabetic animals (blood glucose levels ≥ 220 mg/dL) were post-treated (orally) with NSO (200 and 400 mg/kg) or the standard drug, metformin (150 mg/kg), for 30 days. Two other groups served as the negative and positive controls. NSO significantly (p<0.05) reversed diabetes-induced hyperglycemia, impaired glucose tolerance, dyslipidemia, and oxido-inflammatory imbalances typified by alterations in the NADH/NAD+ ratio (p<0.001), elevations in the levels of C-reactive protein, 4-hydroxynonenal, malondialdehyde, and pro-inflammatory cytokines (TNF-α and Il-1β), and reductions in endogenous antioxidant enzymes. Furthermore, gene expression of inflammatory cytokines and glycogen synthase kinase 3 beta (GSK-3β) was upregulated in the hepatic and pancreatic tissues of NSO-treated animals. The protective effect of NSO was corroborated by the histological assessment of the pancreatic tissue. The results revealed that the anti-diabetic potential of NSO proceeded through its hypolipidemic activity and modulation of redox and inflammatory signaling events in the hepatic and pancreatic tissues.

Chemokines and their receptors play important roles in the pathophysiology of many diseases by regulating the cellular migration of major inflammatory and immune players. The CXC motif chemokine subfamily is the second largest family, and it is further subdivided into ELR motif CXC (ELR+) and non-ELR motif (ELR-) CXC chemokines, which are effective chemoattractants for neutrophils and lymphocytes/monocytes, respectively. These chemokines and their receptors are expected to have a significant impact on a wide range of lung diseases, many of which have inflammatory or immunological underpinnings. As a result, manipulations of this subfamily of chemokines and their receptors using small molecular agents and other means have been explored for potential therapeutic benefit in the setting of several lung pathologies. Furthermore, encouraging preclinical data has necessitated the progression of a few of these drugs into clinical trials in order to make the most effective use of interventions in the development of viable targeted therapeutics. The current review presents the understanding of the roles of CXC ligands (CXCLs) and their cognate receptors (CXCRs) in the pathogenesis of several lung diseases such as allergic rhinitis, COPD, lung fibrosis, lung cancer, pneumonia, and tuberculosis. The potential therapeutic benefits of pharmacological or other CXCL/CXCR axis manipulations are also discussed.

Coronavirus disease 2019 (COVID-19) is a virulent viral disease that has now become a public health emergency of global significance and still without an approved treatment regimen or cure. In the absence of curative drugs and with vaccines development still in progress, alternative approaches to stem the tide of the pandemic are being considered. The potential of a phytotherapeutic approach in the management of the dreaded disease has gained attention, especially in developing countries, with several claims of the development of anti-COVID-19 herbal formulations. This is a plausible approach especially with the increasing acceptance of herbal medicine in both alternative and orthodox medical practices worldwide. Also, the established efficacy of herbal remedies in the treatment of numerous viral diseases including those caused by coronaviruses, as well as diseases with symptoms associated with COVID-19, presents a valid case for serious consideration of herbal medicine in the treatment of COVID-19. However, there are legitimate concerns and daunting challenges with the use of herbs and herbal products. These include issues of quality control, unethical production practice, inadequate information on the composition, use and mechanisms, weak regulatory policies, herb-drug interactions and adverse reactions, and the tendency for abuse. This review discusses the feasibility of intervention with herbal medicine in the COVID-19 pandemic and the need to take proactive measures to protect public health by improving the quality and safety of herbal medicine deployed to combat the disease. Graphical abstract