Browsing by Author "Luqman Aribidesi Olayaki"
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Item Cannabinoid-deficient Benin republic hemp (Cannabis sativa L.) improves semen parameters by reducing prolactin and enhancing anti-oxidant status(BMC Complementary and Alternative Medicine, 2019-06-17) Abdullateef Isiaka Alagbonsi; Luqman Aribidesi Olayaki; Abdulrahim Halimat Amin; Thomson Sijuade Adetona; Gbemileke Tobiloba AkinyemiBackground: Nigerian Cannabis sativa (hemp) causes male gonadotoxicity by inducing hyperprolactinemia, down-regulation of hypothalamic-pituitary-testicular axis, and oxidative stress. Benin republic hemp has been preferred by illicit users in Nigeria but its effect on male fertility is not understood. This study determined and compared the compositions of Benin republic hemp ethanol extract (BHE) and Nigerian hemp. The effects of BHE on semen parameters, reproductive hormones, and anti-oxidant status, and the possibility of bromocriptine (prolactin inhibitor) to abolish hemp-induced toxicities in rats were also investigated. Methods: Thirty-six male Wistar rats were blindly randomized into 6 oral treatment groups (n = 6 each). Groups I (control) and II received normal saline and bromocriptine (3 mg/kg) respectively. Groups III and IV received 2 mg/kg of BHE alone and in combination with bromocriptine respectively, while groups V and VI received 10 mg/kg BHE alone and in combination with bromocriptine respectively. Comparisons among the groups were done by one-way analysis of variance, followed by post-hoc Tukey multiple comparison test. Statistical significance was considered at p < 0.05. Results: The BHE has no cannabichromene and tetrahydrocannabinol but a very small quantity of cannabinol and higher quantity of fatty acids when compared to Nigerian hemp. Both doses of BHE increased sperm count, morphology and viability but not motility. Co-administration of BHE with bromocriptine lowered sperm count but increased sperm morphology and viability. Bromocriptine and/or BHE caused reduction in the plasma prolactin level, increase in the plasma superoxide dismutase activity, but no significant change in the plasma gonadotropin releasing hormone, follicle stimulating hormone (except for the increase in rats that received bromocriptine+ 10 mg/kg BHE), luteinizing hormone, estradiol, malondialdehyde and glutathione peroxidase. The 10 mg/kg BHE or bromocriptine+BHE (both doses) increased total anti-oxidant capacity and catalase. Conclusions: The BHE improves semen parameters by reducing plasma prolactin and enhancing plasma anti-oxidant status. Its pro-fertility potential might be associated with its deficiency in the widely known gonadotoxic phytocannabinoids.Item Cannabis sativa and/or melatonin do not alter brain lipid but alter oxidative mechanisms in female rats(Journal of Cannabis Research, 2021) AbdulRahim Amin Halimat; Isiaka Alagbonsi AbdulIateef; Noah Amuda Oluwasola; Adavize Omeiza; Abdul-Rahuf Aderemi Feyitimi; Luqman Aribidesi OlayakiAbstract Background: Lipid profile and redox status play a role in brain (dys)functions. Cannabinoid and melatonergic systems operate in the brain and contribute to brain (patho)physiology, but their roles in the modulation of brain lipid and redox status are not well-known. We studied the effect of ethanol extract of Cannabis sativa (CS) and/or melatonin (M) on the lipid profile and anti-oxidant system of the rat brain. Methods: We randomly divided twenty-four (24) female Wistar rats into 4 groups (n = 6 rats each). Group 1 (control) received distilled water mixed with DMSO. Groups II–IV received CS (2 mg/kg), M (4 mg/kg), and co- administration of CS and M (CS + M) respectively via oral gavage between 8:00 am and 10:00 am once daily for 14 days. Animals underwent 12-h fasting after the last day of treatment and sacrificed under ketamine anesthesia (20 mg/kg; i.m). The brain tissues were excised and homogenized for assay of the concentrations of the total cholesterol (TC), triacylglycerol (TG), high-density lipoprotein cholesterol (HDL-C), nitric oxide (NO), malondialdehyde (MDA), and the activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and acetylcholinesterase (AChE). One-way analysis of variance (ANOVA) was used to compare means across groups, followed by the least significant difference (LSD) post-hoc test. Results: CS and/or M did not affect the lipid profile parameters. However, CS increased the G6PD (from 15.58 ± 1.09 to 21.02 ± 1.45 U/L; p = 0.047), GPx (from 10.47 ± 0.86 to 17.71 ± 1.04 U/L; p = 0.019), and SOD (from 0.81 ± 0.02 to 0.90 ± 0.01 μM; p = 0.007), but decreased NO (from 9.40 ± 0.51 to 6.75 ± 0.21 μM; p = 0.010) and had no effect on MDA (p = 0.905), CAT (p = 0.831), GR (p = 0.639), and AChE (p = 0.571) in comparison with the control group. M augmented the increase in G6PD (from 21.02 ± 1.45 U/L to 27.18 ± 1.81 U/L; p = 0.032) and decrease in NO (from 6.75 ± 0.21 to 4.86 ± 0.13 μM; p = 0.034) but abolished the increase in GPx (from 17.71 ± 1.04 to 8.59 ± 2.06 U/L; p = 0.006) and SOD (from 0.90 ± 0.01 to 0.70 ± 0.00 μM; p = 0.000) elicited by CS in the rat brain in comparison with the CS group.Item Combination Therapy with Vitamin D and Metformin: A Potential Approach to Mitigate Testicular Dysfunction in Type 2 Diabetes Mellitus(Reproductive Sciences, 2024-09-25) Adeyemi Fatai Odetayo; Halimat Amin Abdulrahim; Adedotun Muiz Yusuf; Williams Oshetename Aromokhame; Ademola Muritala Olaitan; Mirabel Chisom Ugoji; Moses Agbomhere Hamed; Luqman Aribidesi OlayakiType 2 diabetes mellitus (T2DM) is a multifactorial disease that cannot be linked to a single pathway, causing the observed heterogeneity among T2DM patients. Despite this level of heterogeneity, T2DM is majorly managed by metformin (MET) monotherapy. However, recent fndings have associated long-term metformin intake with progressive oxidative pancreatic β cell damage as the disease progresses. Hence, a signifcant number of patients treated with MET need an alternate therapy. Hence, identifying drug combinations that can efectively alleviate diferent diabetes complications would serve as a more promising therapy that can translate into active use. Hence, this study was designed to explore the possible synergistic efect of vitamin D and metformin on T2DM-induced testicular dysfunction. Thirty healthy male Wistar rats (weight: 120-150 g and age: 10 ± 2 weeks) were randomly divided into control, diabetes untreated (HFD+STZ), diabetes + vitamin D (1000 IU/kg), diabetes + metformin (180 mg/kg), and diabetes + vitamin D + metformin. All treatments lasted for 28 days and animals were sacrifced using IP injection of ketamine and xylaxine (40 and 4 mg/kg respectively). Vitamin D improved the ameliorative efect of metformin on T2DM-induced hyperglycemia and lipid dysmetabolism, accompanied by a signifcant decrease in testicular lactate dehydrogenase and lactate. Also, vitamin D + metformin signifcantly increased serum lutein- izing hormone, follicle-stimulating hormone, testosterone, and testicular 5α reductase activities. Furthermore, vitamin D improved the anti-infammatory and antioxidant efects of metformin by signifcantly decreasing T2DM-induced increase in testicular interleukin 1beta, interleukin 6, TNF-α, nitric oxide, and NF-κB and increasing T2DM-induced decrease in interleukin 10, glutathione, superoxide dismutase, catalase, GPx, and Nrf2. Vitamin D enhanced the ameliorative efect of metformin on T2DM-induced testicular dysfunction.Item Elevated, sustained, and yet reversible biotoxicity effects of lead on cessation of exposure: Melatonin is a potent therapeutic option(Toxicology and Industrial Health, 2020-06-03) Wale Johnson Adeyemi; Tahir Ahmad Abdussalam; Amin Abdulrahim; Luqman Aribidesi OlayakiMelatonin (Mel) is known to prevent and mitigate lead (Pb)-induced gonadotoxicity. However, there is no report in literature on the endogenous levels of different biomarkers after the cessation of Pb exposure, with or without treatment with Mel. Fifty adult male Wistar rats were divided into five groups (N 1⁄4 10), which included control ((vehicle (normal saline) - treated) 0.1 ml/day); lead chloride (PbCl2) untreated (3 weeks vehicle þ 3 weeks Pb); Pb recovery (3 weeks Pb þ 3 weeks vehicle); Pb þ Mel (3 weeks Pb þ 3 weeks Mel); and Mel (3 weeks vehicle þ 3 weeks Mel) groups. Pb and Mel were administered at 50 and 10 mg/kg B.W. (p.o.), respectively. The results showed that Pb caused significant decreases in total bilirubin (TB), phospholipids (PLP), superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC), but significant elevations in alkaline phosphatase (ALP), aspartate aminotransferase (AST), triglyceride (TG), and mal- ondialdehyde (MDA). Although the adverse effects of Pb on TB, ALP, AST, SOD, MDA, and TAC were sus- tained after the cessation of exposure, a reversal was observed in total cholesterol (TC), TG, PLP, CAT, and c-reactive protein (CRP) results. Nevertheless, the detrimental effects of Pb on alanine aminotransferase (ALT), albumin, and globulin were only expressed post-exposure. Treatment with Mel caused no significant effect on TB and albumin levels. However, unlike TAC and CRP, the hormone significantly reduced ALP, AST, ALT, TC, low-density lipoprotein cholesterol, PLP, SOD, CAT, MDA, and globulin to levels comparable to the control group. In conclusion, following the cessation of Pb exposure, alterations in physiological balance could be elevated, sustained, or reversible. However, Mel enhanced the reestablishment homeostatic status after Pb administration.Item Melatonin ameliorates ketoconazole-induced increase in thyroid function(Rwanda Journal of Medicine and Health Sciences, 2020-03) Abdullateef Isiaka Alagbonsi,; Luqman Aribidesi Olayaki; Abdulrahim Halimat Amin; Mariam Titilayo Suleiman; Israel Bojuwade; Noah Adavize Omeiza; Sheu Oluwadare SulaimanThe antithyroid effect of ketoconazole has been reported. The secretion and action of melatonin in the thyroid gland are also known. However, the possible effect of melatonin on ketoconazole-induced antithyroid effect is unknown. Objective We sought to investigate the modulatory effect of ketoconazole and/or melatonin on thyroid function in female rats. Methods Groups 1-4 of female rats respectively underwent 14-day treatment with normal saline, 25 mg/kg ketoconazole, 4 mg/kg melatonin and 10 mg/kg melatonin. Groups 5 and 6 both received 14-day treatment with ketoconazole and were respectively treated with 4 mg/kg melatonin and 10 mg/kg melatonin simultaneously. Groups 7 and 8 respectively underwent 14-day pretreatment with 4 mg/kg melatonin and 10 mg/kg melatonin, followed by 14-day administration of ketoconazole to both groups. Groups 9 and 10 were both treated with ketoconazole for 14 days, followed by respective 14-day administration of 4 mg/kg melatonin and 10 mg/kg melatonin. Results TSH, T3, T4, and iodine concentrations were increased by separate administration of ketoconazole and either dose of melatonin when compared to control. However, pre-treatment or post-treatment of ketoconazole- treated rats with melatonin abolished the ketoconazole-induced increase in TSH, T3, T4, and iodine while co-administration of ketoconazole with melatonin caused no improvement in the ketoconazole-induced increase in TSH, T3, and T4 except iodine concentration. Conclusion Ketoconazole increased thyroid function, which was ameliorated by pre- or post-treatment with melatonin, possibly via modulation of the iodination process.Item Melatonin prevents and ameliorates lead-induced gonadotoxicity through antioxidative and hormonal mechanisms(Taxicology And Industrial Health, 2018-04-03) Luqman Aribidesi Olayaki; Isiaka Abdullateef Alagbonsi; Abdulrahim Amin Halimat; Wale Johnson Adeyemi; Muftiat Bakare; Noah OmeizaWe investigated the effects of melatonin on sperm parameters and some biochemical markers in lead- exposed male Wistar rats. Lead (50 mg/kg bw/day) and/or melatonin (4 mg/kg or 10 mg/kg bw/day) was administered for 4 weeks, while 2-week lead exposure was preceded by or followed by 2-week treatment with both doses of melatonin in other groups. Lead reduced glutathione, catalase, adjusted testes weight, semen parameters but did not change malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, and total antioxidant capacity. Though independent of prolactin, lead-induced gonadotoxicity was both centrally and peripherally mediated, as it reduced gonadotropin-releasing hormone and testos- terone levels, while gonadotropin levels did not change significantly probably due to negative feedback by elevated estradiol. However, pre-, simultaneous, or posttreatment of lead-exposed rats with melatonin reduced MDA, SOD, and estradiol but dose-dependently increased other parameters. Conclusively, lead causes male gonadotoxicity through oxidative stress and endocrine mechanisms, and these could be dose- dependently prevented and ameliorated by melatonin.Item Metformin and vitamin D combination therapy ameliorates type 2 diabetes mellitus‐induced renal injury in male Wistar rats(Naunyn-Schmiedeberg's Archives of Pharmacology, 2024-09-30) Halimat Amin Abdulrahim; Emmanuel Aduragbemi Owootori; Adeyemi Fatai Odetayo; Joshua Damrah Bulus; Fatimoh Bolanle Jimoh; Emmanuel Oluwamuyiwa Gabriel; Iyanu Feranmi Odiete; Luqman Aribidesi OlayakiDiabetic kidney disease is a major microvascular diabetes mellitus (DM) complication clinically associated with a gradual renal function decline. Although metformin is a common drug for managing DM, however, monotherapy treatment with any antidiabetic drug will necessitate dosage increment since type 2 DM (T2DM) deteriorates over time due to the increasing pancreatic β-cell dysfunction and will eventually require a combination therapy approach with another antidiabetic medica- tion. Vitamin D is a food supplement that has been proven to have antidiabetic and reno-protective activities. Hence, we explore the combination of vitamin D and metformin on T2DM-induced renal dysfunction. Thirty male Wistar rats were randomized into fve (5) groups: control, diabetes untreated, diabetics treated with metformin, vitamin D, and vitamin D+metformin. Vitamin D and metformin signifcantly reversed DM-induced hyperglycemia, electrolyte imbalance, and dyslipidemia. Also, vitamin D and metformin reversed T2DM-induced increase in serum creatinine and urea and renal lactate, LDH, and oxido-infammatory response. These observed alterations were accompanied by an increase in proton pump activities and modulation of Nrf2/Nf-κB and XO/UA signaling. This study revealed that vitamin D and/or metformin ameliorated T2DM-induced renal injury.Item Physical exercise improved the hematological effect of vitamin D in type 2 diabetes mellitus-induced nephrotoxicity in rats(Biochemistry and Biophysics Reports, 2024-12) Amin Abdulrahim Halimat; Adeyemi Fatai Odetayo b; Adeoye Tunwagun David; Yusuf Funsho Abdulquadri; Rofiat Oluwasheun Sheu; Pelumi Kikelomo Oluwafemi; Kazeem Bidemi Okesina; Luqman Aribidesi OlayakiIntroduction: Globally, one of the major causes of renal dysfunction is diabetes mellitus (DM), and diabetic- induced nephrotoxicity has been linked with anemia. Presently, numerous antidiabetic drugs have been designed for the management of this disorder but they possess their undesirable effects such as anemia and acute kidney injury. Hence, we explore the use of vitamin D with or without exercise for the management of DM- induced renal dysfunction. Methods: Thirty-six (36) Wistar rats were randomly separated into six (6) groups: control (vehicle treated), diabetes untreated (HFD + STZ), diabetes + vitamin D (HFD + STZ + vitamin D), diabetes + exercise (HFD + STZ + exercise), diabetes + vitamin D + exercise (HFD + STZ + vitamin D+ exercise), diabetes + metformin (HFD + STZ + metformin). Results: Vitamin D with or without exercise significantly reduced T2DM-induced hyperglycemia. Also, a decrease in T2DM-induced increase in urea, creatinine, lactate dehydrogenase, lactate, cholesterol, and triglyceride and a rise in DM-associated reduction in high-density lipoprotein. These events were associated with a significant increase in red blood cells, hematocrit value, hemoglobin, erythropoietin, and a decrease in white blood cell count. Furthermore, vitamin D with or without exercise reversed T2DM-induced increase in pro-oxidant and pro- inflammatory markers. This observed oxido-inflammatory response was associated with a significant increase in xanthine oxidase activities and uric acid concentration. Interestingly, better recovery rates from DM-associated hematological imbalance were discovered in rats co-treated with vitamin D and exercise. Conclusion: Our findings revealed that exercise enhanced the hematological effect of vitamin D in HFD + STZ- induced T2DM animals.Item Synergistic Effects of Vitamin D and Exercise on Diabetes-induced Gonadotoxicity in Male Wistar Rats: Role of Xanthine Oxidase/Uric Acid and Nrf2/NfkB Signaling(Cell Biochemistry and Biophysics, 2024-05-13) Adeyemi Fatai Odetayo; Abdulrahim Halimat Amin; Olaoluwa Tolulope Fabiyi; Taiye Abdulmujeeb Adewole; Bright Elijah Ajiboye; Adavize Noah Omeiza; Luqman Aribidesi OlayakiType 2 Diabetes mellitus (T2DM) is one of the oldest known chronic diseases, characterized by elevated fasting blood sugar (FBS). T2DM is a metabolic disorder that can distort the activities of multiple physiological systems, including the reproductive system. Although different drugs have been designed for managing this disorder, these drugs have been reported to have negative side effects. Hence, this study was designed to explore the possible synergistic effect of vitamin D and exercise on T2DM-induced testicular dysfunction. Thirty-six male Wistar rats were randomized into six (6) groups: control, diabetes untreated, diabetes treated with 1000 IU/kg of vitamin D, diabetes treated with 5 min/day of physical exercise, diabetes treated with vitamin D and exercise, diabetes treated with 180 mg/kg of metformin. T2DM induction led to a significant increase in FBS, lactate, and lactate dehydrogenase, and was reversed by vitamin D supplementation and exercise. Also, vitamin D and exercise synergistically blunted T2DM-induced oxido-inflammatory response evidenced by a significant decrease in testicular malondialdehyde, interleukin 1β, interleukin 6, and tumor necrosis factor alpha, and an increase in superoxide dismutase, catalase, glutathione peroxidase, and interleukin 10. These events were associated with a decrease in T2DM-induced increase in XO, UA, and Nf-κb and an increase in T2DM-induced decrease in Nrf2. Also, vitamin D and EX reversed the observed impairment in sperm quality and testicular histology following T2DM-induction. This study revealed the synergistic effect of vitamin D and exercise on T2DM-induced testicular dysfunction.