Pausinystalia yohimbe (P. yohimbe) stem bark powder is commonly used as seasoning for barbecue beef in Nigeria and some West African countries. This study evaluated the effect of ingesting ethanol extract of P. yohimbe stem bark on some hormones and tissues linked with fertility in female Wistar rats. A total of fifteen adult female Wistar rats weighing between 140 - 160g were used for this study after an initial Acute Toxicity test was done to establish a safe dose range of the extract. The animals were randomly divided into three groups of five rats per group. Group 1 served as control and received normal saline while Groups 2 and 3 received 400 mg/kg and 800 mg/kg body weight (bw) of ethanol extract of P. yohimbe stem bark respectively, via oral gavage, for 21 days. At the end of the treatment period, the rats were weighed, sacrificed and blood, ovary and uterus samples collected for determination of reproductive hormones (follicle-stimulating hormone, estrogen, and progesterone) and histological examination using standard methods. The results showed that LD50 of the ethanol extract for the female Wistar rats was 3807.89 mg/kg bw. There were significant (p˂0.05) increases in body weight, estrogen and follicle-stimulating hormone (FSH) of the treated groups compared with the control. Histological examination also showed degenerative changes in the uterus of the rats in groups 2 and 3, with no alterations in the ovary when compared to control. These results suggest that continuous consumption of ethanol extract of P. yohimbe stem bark may alter the systemic concentration of estrogen and follicle-stimulating hormone as well as morphology of the uterus which may lead to reduced reproductive function and female infertility.
Pausinystalia yohimbe is a medicinal plant widely used as an aphrodisiac agent in Nigeria and other parts of West Africa, but little is known about its effect on renal function after chronic use. This study was designed to investigate the effect of ethanolic extract of Pausinystalia yohimbe stem bark on renal function parameters such as serum creatinine, urea, electrolyte, oxidative stress markers, and hematological parameters in female Wistar rats. Ethanolic extract of Pausinystalia yohimbe stem bark was administered orally to 3 groups of 5 female rats for 21 days as follows: group1 which served as control received distilled water while groups 2 and 3 received 400mg/kg and 800mg/kg body weight of the extract respectively. Thereafter the rats were sacrificed, and blood and kidney tissues were collected for biochemical analysis. The result showed that there were no significant changes in urea, creatinine, potassium, chloride, and bicarbonate levels while sodium level was significantly increased (p<0.05) when compared to the control. SOD and CAT tissue activities did not show any significant change (p<0.05) while there was a significant increase (p<0.05) in GSH and a significant reduction (p<0.05) in MDA. Also, there was no significant change (p<0.05) in WBC, PCV, and platelets, however, there was a significant decrease (p<0.05) in RBC and hemoglobin levels. The histopathology of the kidney showed that no significant changes were observed between treatment groups and control except for the 800 mg/kg body weight of the extract-treated group where there was mild multifocal vacuolar degeneration of some renal tubular epithelial cells. The result suggests that the chronic use of the ethanolic extract of Pausinystalia yohimbe stem bark protects the kidney against oxidative stress but adversely affects the functional capacities of the kidney and formation of erythropoietin in the stem cells and may also contribute to the increasing number of persons with high blood pressure.
This study explored the protective potential of apocyanin and curcumin in diclofenac-induced cardiotoxicity utilizing cardiac enzymes, pro-inflammatory markers, and along with histopathological endpoints. A total of 123 male Wistar rats were used for the study. 43 rats were used for the determination of the median lethal dose (LD50) of apocyanin and curcumin while 80 rats were randomly divided into 8 groups of 10 rats each. Group 1(control) received distilled water while others received orally, per mg/kg body weight of treatments as follows: group 2(1000, apocyanin, group 3(1000, curcumin), group 4(10, diclofenac), group 5(500, apocyanin and 10, diclofenac), group 6(1000, apocyanin and 10, diclofenac), group 7(500, curcumin and 10, diclofenac) and group 8(1000, curcumin and 10, diclofenac). The treatments were administered daily for 14 and 28 days. LD50 up to 5000mg/kg body weight of apocyanin and curcumin did not show any fatality in animals. Administration of diclofenac significantly (p < 0.05) elevated the activities of creatinine kinase-MB, lactate dehydrogenase, levels of troponin-T, and tumor necrosis factor. There was no alteration in the activities of Interleukin- 1β. The histological results also showed cardiac insults such as cardiac muscle having severe fibro collagenous stroma, reduced myocytes density, and thick wall blood vessels. However, pretreatment with 500 and 1000 mg/kg body weight of apocyanin or curcumin attenuated all biochemical alterations and histological lesions induced by diclofenac in a dose-dependent manner. Pretreatments with apocyanin and curcumin inhibitors of NADPH oxidases 2weres effective in ameliorating diclofenac-induced cardiotoxicity suppressing inflammation and restoring normal histological architecture, thus, highlighting the therapeutic potentials of apocyanin and curcumin in the management of diclofenac-mediated cardiotoxicity.
This study explored the protective potential of NADPH-oxidase inhibitors, apocynin and curcumin in diclofenac-induced cardiotoxicity via oxidative stress. A total of 80 male Wistar rats were used for the study. 80 rats were randomly divided into 8 groups of 10 rats each. Group 1(control) received distilled water while others received orally, per mg/kg body weight of treatments as follows: group 2(1000, apocynin, group 3(1000, curcumin), group 4(10, diclofenac), group 5(500, apocynin and 10, diclofenac), group 6(1000, apocynin and 10, diclofenac), group 7(500, curcumin and 10, diclofenac) and group 8(1000, curcumin and 10, diclofenac). The treatments were administered daily for 14 and 28 days. Administration of diclofenac significantly (p<0.05) elevated the activities of NAD(P)H oxidases type 2 and malondialdehyde while the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione level were significantly (p<0.05) decreased. There was no alteration in the activities of xanthine oxidase. However, pretreatment with 500 and 1000 mg/kg body weight of apocynin or curcumin attenuated all biochemical alterations induced by diclofenac in a dose dependent manner. Pretreatments with apocynin and curcumin inhibitors of NOX 2 was effective in ameliorating diclofenac-induced cardiotoxicity by alleviating the oxidative stress thus, highlighting the therapeutic potentials of apocynin and curcumin in the management of diclofenac-mediated cardiotoxicity.
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