Search

Cadmium (Cd) is a heavy metal that is deleterious to brain development as it increases brain aging. Trévo is a multi-herbal supplement that provides various health benefits, including boosting the immune system and detoxification. In this study, we investigated the neuroprotective effects of Trévo against the neurotoxic effects of cadmium chloride (CdCl2). Thirty male Wistar rats were equally divided into three groups: Group I (normal control), Group II (administered CdCl2), and Group III (administered Trévo and CdCl2), and were used in the experiments. Animals were pretreated with 2 mL/kg of Trévo for five days and injected with Cd intraperitoneally 3 h later. Cd significantly increased the production of malondialdehyde (MDA), amyloidogenesis, activation of caspase 3 and 9, and the production of p53 and glutamate. It also inhibited the activity of Na+/K+ ATPase, glutamate dehydrogenase, catalase, superoxide dismutase, and glutathione-S-transferase. The administration of Trévo revealed its antioxidant, anti-amyloidogenic, anti-excitotoxicity, and anticholinesterase properties as it prevented the biochemical changes induced by Cd toxicity in the brain of male Wistar rats. Our results supported the reported health benefits of Trévo as a good dietary supplement in preventing the toxic effects of poisonous substances, such as cadmium.

The current work investigated the chemical profile, antimalarial potential and capacity of hydroethanolic

Amos Sunday Onikanni,1– 3,* Bashir Lawal,4,5,* Augustine O Olusola,1 Janet O Olugbodi,6 Saidu Sani,7 Basiru Olaitan Ajiboye,8 Omotayo B Ilesanmi,9 Mohammed Alqarni,10 Gomaa Mostafa-Hedeab,11,12 Ahmad J Obaidullah,13,14 Gaber El-Saber Batiha,15 Alexander TH Wu16– 21 1Toxicology and Environmental Laboratory, Department of Biochemistry, Faculty of Science, Adekunle Ajasin University, Akungba-Akoko, Ondo State, Nigeria; 2Biochemistry Unit, Department of Chemical Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria; 3Graduate Institute of Biomedical Science, College of Medicine, China Medical University, Taipei, Taiwan; 4PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, 11031, Taiwan; 5Graduate Institute of Cancer Biology & Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, 11031, Taiwan; 6Department of Biochemistry, Bingham University, Karu, Nigeria; 7Department of Biochemistry, Faculty of Biological Science, Alex Ekwueme Federal University Ndufu Alike IkwoD, Abakaliki, Ebonyi State, Nigeria; 8Phytomedicine and Molecular Toxicology Research Laboratory, Department of Biochemistry, Faculty of Science, Federal University, Oye-Ekiti, Ekiti State, Nigeria; 9Department of Biochemistry, Faculty of Science, Federal University Otuoke, Ogbia, Bayelsa State, 23401, Nigeria; 10Department of Pharmaceutical Chemistry, College of Pharmacy, Taif University, Taif, 21944, Saudi Arabia; 11Pharmacology Department & Health Research Unit, Medical College, Jouf University, Sakakah, Saudi Arabia; 12Pharmacology Department, Faculty of Medicine, Beni-Suef University, Beni Suef, Egypt; 13Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh, 11451, Saudi Arabia; 14Drug Exploration and Development Chair (DEDC), Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh, 11451, Saudi Arabia; 15Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt; 16The PhD Program of Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, 11031, Taiwan; 17International Ph.D. Program for Translational Science, College of Medical Science and Technology, Taipei Medical University, Taipei, 11031, Taiwan; 18TMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei, 11031, Taiwan; 19Clinical Research Center, Taipei Medical University Hospital, Taipei Medical University, Taipei, 11031, Taiwan; 20Taipei Heart Institute, Taipei Medical University, Taipei, 11031, Taiwan; 21Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, 11490, Taiwan*These authors contributed equally to this workCorrespondence: Alexander TH Wu Tel +886 2 2697 2035Email chaw1211@tmu.edu.twBackground: Sterculia tragacantha is a medicinal plant commonly used in the western part of Nigeria, for managing diabetes mellitus. However, there is a dearth of scientific information on the antidiabetic and neuroprotective properties of the plant.Methods: The in silico, in vitro and in vivo models were used to evaluate the antioxidants, antidiabetic, anti-inflammatory and neuroprotective potential of aqueous extract of Sterculia tragacantha leaf (AESTL) in streptozotocin (STZ)-induced diabetic rats. Thirty (30) male albino rats (155.34± 6.33 g) were intraperitoneal injected with 40 mg/kg of freshly prepared streptozotocin and were divided into 5 groups (A-E) of 6 animals each. Groups A–D were treated with 0, 150 and 300 mg/kg of AESTL, and 200 mg/kg body weight of metformin respectively, while group E serve as the normal control.Results: The results of in vitro analysis revealed dose-dependent antioxidant activities; ABTS (IC50 = 63.03± 2.57 μg/mL), DPPH (117.49± 2.35 μg/mL), FRAP (15.19± 0.98 mmol/100g), TAC (43.38± 0.96 mg/100g), hypoglycaemic effect; α-amylase (IC50 = 77.21± 4.35 μg/mL) and α-glucosidase (IC50 = 443.25± 12.35), and anti-cholinesterase; AChE (IC50 = 113.07± 3.42 μg/mL) and BChE (IC50 = 87.50± 4.32 μg/mL) activities of AESTL. In vivo study revealed dose-dependent hypoglycemic effect and body weight improvement in rats treated with the AESTL. In addition, AESTL improved the antioxidant status and attenuated STZ-induced dysregulations of Na+-K+-ATPase, cholinesterases and neurotransmitters in the brain tissue of experimental rats. The results also demonstrated that AESTL could regulate anti-inflammatory response via inhibition of COX-2/NO signaling axis in the brain of diabetic rats. Molecular docking analysis revealed that epicatechin and procyanidin B2, the bioactive compounds from AESTL, docked well to the binding cavities of acetylcholinesterase, butyrylcholinesterase, α-amylase and α-glucosidase with binding affinities ranges between – 8.0 and – 11.4 kcal/mol, suggesting that these compounds are the bioactive component that could be responsible for the antidiabetic and neuroprotective activities of AESTL.Conclusion: The results of the present study strongly suggested that the AESTL extract could be very useful for halting diabetes progression and its associated neuroinflammation complications.Keywords: Sterculia tragacantha, cholinesterase, antidiabetic, neurotransmitters, oxidative stress markers

Lead exposure has been linked to health challenges involving multiple organ failure. More than fifty percent of lead present in the human body is accumulated in the liver causing hepatic injury. A major mechanism of lead toxicity is oxidative stress. TrévoTM is a nutritional supplement with numerous bioactive natural products with detoxifying and antioxidant properties. This study was designed to investigate the hepatoprotective effects of TrévoTM dietary supplements against lead-hepatotoxicity in male Wistar rats. Thirty-five healthy animals were divided into five groups of seven each as follows: Group I=control; II=15 mg/kg of lead acetate (PbA); III= 2 mL/kg of TrévoTM + PbA; IV= 5 mL/kg of TrévoTM + PbA;V=5 mL/kg of TrévoTM . Animals were orally treated with TrévoTM for two days before co-administration with PbA intraperitoneally for 12 consecutive days. Animals were sacrificed 24 h after the last administration and blood were collected via cardiac puncture and processed for hematological parameters and assessment of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB). The liver was excised and processed for markers of oxidative stress and histopathological examination. Intraperitoneal administration of 15 mg/kg of PbA caused a significant increase in serum concentration of AST, ALT, while the concentration of ALB was significantly decreased (P

The current work investigated the chemical profile, antimalarial potential and capacity of hydroethanolic Senna alata extract (SAE) to reverse hematological and biochemical pertubation in Plasmodium berghei infected mice. Results of the phytochemical analysis revealed the presence of alkaloids, flavonoids, phenolics, tannins, terpenoids, saponins, steroids and cardiac glycosides. Total phenolic and flavonoid content was estimated to be 45.29 ± 2.34 mg GAE/g and 25.22 ± 2.26 mg QE/g respectively. In vitro analysis of the extract also confirmed its antioxidant property. Results of the test for prophylaxis of P. berghei indicated that SAE suppressed parasitemia significantly in treated groups in a dose dependent manner when compared with negative control group. Similarly, SAE improved the mean survival time (MST) and packed cell volume (PCV) of infected mice. The test for curative effect showed that SAE significantly suppressed parasitemia to 4.50 ± 1.05% compared to untreated group 29.83 ± 3.49%. Results of liver and kidney functions indices of treated animals indicated that whereas infection with P. berghei caused increase in the levels of AST, ALT, ALP, urea and creatinine, treatment with SAE significantly reversed the perturbation. Similarly, infected mice were dyslipidemic with concomitant increased activity of HMG CoA reductase and decreased activity of antioxidant enzymes with increase in lipid peroxides levels. However, these alterations were significantly reversed by administration of SAE. Results of this study shows that Senna alata possess antimalarial activity and therefore justify the traditional use of plant for the treatment of malaria.