African walnut (Tetracarpidium conophorum) extract upregulates glucocerebrosidase activity and circumvents Parkinsonian changes in the Hippocampus via the activation of heatshock proteins.

BACKGROUND: Neurodegenerative illnesses like Parkinson's and Alzheimer's are largely caused by the accumulation of aggregated proteins. Heat shock proteins (HSPs), which are molecular chaperons, have been linked with the modulation of ß-glucocerebrosidase (GCase) function encoded by GBA1 and Synucleinopathies. Herein, the chaperonic properties of African walnut ethanolic extract (WNE) in manganese-induced Parkinsonian neuropathology in the hippocampus was examined. METHODOLOGY: 48 adult male rats weighing 185 g ± 10 g were randomly assigned into 6 (A - F) groups (n = 8) and treated orally as follows: A-PBS (1 ml daily for 28 days), B-WNE (200 mg/kg daily for 28 days), C- WNE (400 mg/kg daily for 28 days), D-Mn (100 mg/kg daily for 28 days), E-Mn plus WNE (100 mg/kg Mn + 200 mg/kg WNE daily concomitantly for 28 days), F-Mn plus WNE (100 mg/kg Mn + 400 mg/kg WNE daily concomitantly for 28 days). RESULTS: Rats treated with WNE showed increased levels of HSP70 and HSP90 in comparison with the Mn-intoxicated group. GCase activity also increased significantly in animals treated with WNE. Our results further revealed the therapeutic tendencies of WNE against Mn toxicity by modulating oligomeric α-synuclein levels, redox activity, and glucose bioenergetics. Furthermore, immunohistochemical evaluation revealed reduced expression of neurofibrillary tangles, and reactive astrogliosis following WNE treatment. CONCLUSION: The ethanolic extract of African Walnut induced the activation of HSPs and increased the expression of GBA1 gene in the hippocampus. Activated heat shock proteins suppressed neurodegenerative changes due to Manganese toxicity. WNE was also shown to modulate neuroinflammatory, bioenergetics and neural redox balance in Parkinson-like neuropathology. This study was limited to the use of crude walnut extract and the evaluation of non-motor cascades of Parkinson's disease.

Hepatoprotective effects of Quassia amara stem bark against cadmium-induced toxicity in male Wistar rats.

OBJECTIVES: The liver is one of the primary biorepositories of cadmium (Cd) and it has been implicated in the pathogenesis of hepatic diseases. Quassia amara stem bark has been reputed to have strong antimalarial, antimicrobial, antiulcerative and amoebicidal properties. This study aims to determine the effects of Q. amara on Cd-induced hepatotoxicity and lipid profile in male Wistar rats. METHODS: The animals were divided into three groups of five animals each. Group 1 served as control while group 2 received Cd (5 mg/kg) for 4 weeks. Prior to Cd treatment, group 3 was treated with Q. amara extract (200 mg/kg) for 2 weeks and received the Q. amara and Cd simultaneously for 4 weeks. RESULTS: Cadmium caused significant increase in serum total cholesterol and low-density lipoprotein (LDL) as well as increased hepatic malondialdehyde (MDA) when compared with the control group. On the other hand, Cd caused a decrease in serum high-density lipoprotein (HDL) and hepatic superoxide dismutase (SOD) when compared with control. However, treatment with Q. amara prevented Cd-induced changes in the lipid profile, augmented Cd-induced decline in SOD and also ameliorated the Cd-induced increase in MDA. Catalase level was however comparable across the groups. CONCLUSIONS: Q. amara ameliorated the Cd-induced damage to liver by preventing dyslipidemia and oxidative damage in the hepatic tissue.

Buchholzia coriacea (wonderful kola) seeds induce male reproductive toxicity by suppressing the pituitary-gonadal axis in Wistar rats

The methanolic extract of Buchholzia coriacea seeds (MEBC) has been reported to induce male reproductive toxicity by decreasing sperm parameters and fertility index. To elucidate the possible mechanism(s), the effects of graded doses of MEBC on sex hormones and sperm profile were investigated in this study. The MEBC (e.g., 50, 200, 400, and 600 mg/kg) was administered daily (p.o.) to male Wistar rats for 6 weeks, while a concurrent control group received distilled water (vehicle). Then, the animals were sacrificed under sodium pentobarbital anaesthesia. Weights of organs were recorded, and the sperm profile was determined microscopically. Testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) were assayed from the obtained serum using the ELISA technique. Sperm motility was significantly reduced by MEBC (i.e., 50 and 200 mg/kg), and sperm count reduced in all treated groups in a dose-dependent manner compared with that of the control. Serum testosterone, LH, and FSH decreased in treated rats. A histopathological examination of testes showed a considerable depletion and necrosis of the epithelium of seminiferous tubules. The result suggests that Buchholzia coriacea seeds induce male reproductive toxicity by suppressing the pituitary-gonadal axis.

Effects of aqueous extract of Moringa oleifera seed on cadmium-induced reproductive toxicity in male Wistar rats.

BACKGROUND: Moringa oleifera seeds have been reported to increase sexual activity of male rats but its mechanism of action remains unknown. OBJECTIVE: Cadmium is a heavy metal that induces reproductive toxicity. To elucidate its possible mechanisms of action, the effects of aqueous extract of Moringa seeds (AEMS) on Cadmium-induced reproductive damage were investigated. METHODS: Thirty male rats (180-200g, n=5) were grouped as follows: Control, Cadmium (2mg/kg), AEMS (100 and 500mg/kg), Cadmium+100mg/kg AEMS and Cadmium+500mg/kg AEMS. Single intraperitoneal dose of Cadmium was administered while AEMS was given daily (p.o) for 6 weeks and thereafter sacrificed by cervical dislocation. Sperm variables were examined microscopically while serum was analysed for sex hormones and antioxidants, testicular and epididymal total protein from tissue homogenate. Data were analysed using Students t-test and ANOVA. RESULTS: Cadmium caused significant decrease in sperm variables. The AEMS decreased sperm motility, count and testosterone. These declines were dose dependent. Total testicular protein was significantly lowered by AEMS but total epididymal protein was not affected. Serum catalase and SOD was reduced by AEMS while MDA increased. CONCLUSION: Moringa seeds may exhibit male reproductive toxicity, as observed from its deleterious effect on androgen and sperm variables. It failed to prevent cadmium-induced alteration in reproductive variables and serum antioxidants.