Browsing by Author "Ogunmiluyi, I. O."

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Antihypertensive Power of Naringenin is Mediated via Attenuation of Mineralocorticoid Receptor (MCR)/ Angiotensin Converting Enzyme (ACE)/ Kidney Injury Molecule (Kim-1) Signaling Pathway
(Elsevier B.V, 2020) Oyagbemi, A. A.; Omobowale, T. O.; Adejumobi, O. A.; Owolabi, A. M.; Ogunpolu, B. S.; Falayi, O. O.; Hassan, F. O.; Ogunmiluyi, I. O.; Asenuga, E. R.; Ola-Davies, O. E.; Soetan, K. O.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. J.; Oguntibeju, O. O.; Yakubu, M. A.
Hypertension is a condition with chronic elevation of blood pressure and a common preventable risk factor for cardiovascular disease with attendant global morbidity and mortality. The present study investigated the novel antihypertensive and neuroprotective effect of Naringenin on L-NG-Nitro arginine methyl ester (L-NAME) induced hypertension together with possible molecular mechanism of action. Rats were divided into four groups. Rats in Group A were normotensive. The hypertensive group (Group B) received 40 mg/kg of L-NAME alone while Groups C and D were concurrently administered Naringenin (50 mg/kg) or Lisinopril (10 mg/kg) together with L-NAME orally for 3 weeks. Blood pressure parameters, markers of oxidative stress and renal damage were measured. The immunohistochemistry of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme were also determined. Results indicated significant increases in malondialdehyde, advanced oxidation protein products, protein carbonyl contents and decrease in serum nitric oxide bioavailability in hypertensive rats. Furthermore, there were significant increases in serum myeloperoxidase, urinary creatinine, albumin and blood urea nitrogen in hypertensive rats in comparison to hypertensive rats treated with either Naringenin or Lisinopril. Immunohistochemistry revealed significant expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme in hypertensive rats. However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Collectively, Naringenin offered a novel antihypertensive and neuroprotective effect through downregulation of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme.
Clofibrate, a peroxisome proliferator-activated receptor-alpha (PPARα) agonist, and its molecular mechanisms of action against sodium fluoride-induced toxicity
(Springer Nature, 2021) Oyagbemi, A. A.; Adejumobi, O. A.; Jarikre, T. A.; Ajani, S. O.; Asenuga, E. R.; Gbadamosi, I. T.; Adedapo, A. D. A.; Aro, A. O.; Ogunpolu, B. S.; Hassan, F. O.; Falayi, O. O.; Ogunmiluyi, I. O.; Omobowale, T. O.; Arojojoye, O. A.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Emikpe, B. O.; Oyeyemi, M. O.; Nkadimeng, S. M.; McGaw, L. J.; Kayoka-Kabongo, P. N.; Oguntibeju, O. O.; Yakubu, M. A.
Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating fluoride-induced hypertension and nephrotoxicity with clofibrate, a peroxisome proliferator–activated receptor-alpha (PPARα) agonist. For this study, forty male Wistar rats were used and randomly grouped into ten rats per group, control, sodium fluoride (NaF; 300 ppm) only, NaF plus clofibrate (250 mg/kg) and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. The administration of NaF was by drinking water ad libitum, while clofibrate and lisinopril were administered by oral gavage. Administration of NaF induced hypertension, and was accompanied with exaggerated oxidative stress; depletion of antioxidant defence system; reduced nitric oxide production; increased systolic, diastolic and mean arterial pressure; activation of angiotensin-converting enzyme activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); and testicular apoptosis. Treatment of rats with clofibrate reduced oxidative stress, improved antioxidant status, lowered high blood pressure through the inhibition of angiotensin-converting enzyme activity, mineralocorticoid receptor over-activation, and abrogated testicular apoptosis. Taken together, clofibrate could offer exceptional therapeutic benefit in mitigating toxicity associated with sodium fluoride.
In vitro cytotoxicity activity of the methanol leaf extract of Picralima nitida on human colorectal adenocarcinoma cell lines (HT-29)
(AkiNik Publications, 2021) Adedapo, A. A.; Yusuff, A. A.; Falayi, O. O.; Ogunmiluyi, I. O.; Ogunpolu, B. S.; Omobowale, T. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Oguntibeju, O. O.; Yakubu, M. A.; Yakubu, F. B.
The anti-proliferative effect of the methanol leaf extract of Picralima nitida on Human Colorectal Adenocarcinoma Cell lines (HT-29) was investigated using the Cell Titer 96 MTT assay because Picralima nitida is a therapeutic herb used in ethnomedicine for the management of several disease conditions. Cells were cultured to confluence, trypsinized, and plated in 96-well plates for cell proliferation assay. Twenty four hours after plating, cells were treated with various concentrations (62.5, 125, 250 μm) of the extract along with the control in the presence or absence of Calphostin C (10 μm) or Tyrphostin (10 μm) and cultured for 24–72 h to determine effects of treatment on cell growth. MTT assay was performed at 24, 48 and 72. MTT assay was performed over 3 days. In vitro antiproliferative study showed that the extract at all concentrations caused cytotoxicity of the HT29 cells. The extract in the absence of the enzyme inhibitors caused a higher cell inhibition than in their presence with the 62.5 μm/ml causing a higher inhibitory effect on the cells. The ability of the methanol leaf extract of Picralima nitida with a higher antiproliferative property in the absence of the enzyme inhibitors is a pointer to its cytotoxic efficacy. It was thus concluded from this study that the plant extract from Picralima nitida has anti-proliferative/cytotoxic effect hence further evaluation on the constituents responsible for this effect may be explored.
Potential health benefits of zinc supplementation for the management of the COVID-19 pandemic
(Wiley, 2020) Oyagbemi, A. A.; Ajibade, T. O.; Aboua, Y. G.; Gbadamosi, I. T.; Adedapo, A. D. A.; Aro, A. O.; Adejumobi, O. A.; Thamahane-Katengua, E.; Omobowale, T. O.; Falayi, O. O.; Oyagbemi, T. O.; Ogunpolu, B. S.; Hassan, F. O.; Ogunmiluyi, I. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. J.; Kayoka-Kabongo, P. N.; Oguntibeju, O. O.; Yakubu, M. A.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent for the Coronavirus Disease 2019 (COVID-19). The COVID-19 pandemic has created unimaginable and unprecedented global health crisis. Since the outbreak of COVID-19, millions of dollars have been spent, hospitalization overstretched with increasing morbidity and mortality. All these have resulted in unprecedented global economic catastrophe. Several drugs and vaccines are currently being evaluated, tested, and administered in the frantic efforts to stem the dire consequences of COVID-19 with varying degrees of successes. Zinc possesses potential health benefits against COVID-19 pandemic by improving immune response, minimizing infection and inflammation, preventing lung injury, inhibiting viral replication through the interference of the viral genome transcription, protein translation, attachment, and host infectivity. However, this review focuses on the various mechanisms of action of zinc and its supplementation as adjuvant for vaccines an effective therapeutic regimen in the management of the ravaging COVID-19 pandemic.
The therapeutic potential of the novel angiotensin-converting enzyme 2 in the treatment of coronavirus disease 2019 (COVID-19)
(Horizon Publisher India, 2021) Oyagbemi, O. A.; Ajibade, T. O.; Abowa, Y. G.; Gbadamosi, I. I.; Adedapo, A. D. A.; Aro, A. O.; Adejumobi, O. A.; Thamahane-Katenuga, E.; Omobowale, T. O.; Falayi, O. O.; Oyagbemi, T. O.; Ogunpolu, B. S.; Hassan, F. O.; Ogunmiluyi, I. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. Z.; Kayoka-Kabongo, P. N.; Yakubu, M. A.; Oguntibeju, O. O.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). This virus has become a global pandemic with unprecedented mortality and morbidity along with attendant financial and economic crises. Furthermore, COVID-19 can easily be transmitted regardless of religion, race, sex, or status. Globally, high hospitalization rates of COVID-19 patients have been reported, and billions of dollars have been spent to contain the pandemic. Angiotensin-converting enzyme (ACE) 2 is a receptor of SARS-CoV-2, which has a significant role in the entry of the virus into the host cell. ACE2 is highly expressed in the type II alveolar cells of the lungs, upper esophagus, stratified epithelial cells, and other tissues in the body. The diminished expressions of ACE2 have been associated with hypertension, arteriosclerosis, heart failure, chronic kidney disease, and immune system dysregulation. Overall, the potential drug candidates that could serve as ACE2 activators or enhance the expression of ACE2 in a disease state, such as COVID-19, hold considerable promise in mitigating the COVID-19 pandemic. This study reviews the therapeutic potential and pharmacological benefits of the novel ACE2 in the management of COVID-19 using search engines, such as Google, Scopus, PubMed, and PubMed Central.