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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

We earlier reported the protective effect of Solanum dasyphyllum against cyanide neurotoxicity. In furtherance to this, we investigated the protective effect of S. dasyphyllum against rotenone, a chemical toxin that causes brain-related diseases. Mitochondria fraction obtained from the brain of male Wistar rats was incubated with various solvents (hexane, dichloromethane, ethylacetate, and methanol) extracts of S. dasyphyllum before rotenone exposure. Mitochondria respiratory enzymes (MRE) were evaluated along with markers of oxidative stress. The inhibition of MRE by rotenone was reversed by treatment with various fractions of S. dasyphyllum. The oxidative stress induced by rotenone was also reversed by fractions of S. dasyphyllum. In addition, the ethylacetate fraction of S. dasyphyllum was most potent against rotenone-induced neurotoxicity. In conclusion, S. dasyphyllum is rich in active phytochemicals that can prevent some neurotoxic effects of rotenone exposure. Further study can be done in an in vivo model to substantiate our results.

Potassium cyanide (KCN) is a salt that release cyanide upon degradation in living system. Cyanide is a chemical that induced its toxicity and lethal effect through the inhibition of cytochrome C oxidase activity. Trevo, a phytochemical rich product is majorly used for its antiaging and disease prevention among individuals. We evaluated the potential of trevo to reverse the biochemical toxicity of cyanide in the brain of male wistar rats. The biochemical changes assessed are- cytochrome C oxidase (CCO), neurochemicals (acetylcholine esterase (ACHE), dopamine and serotonin), and p53, antioxidants (catalase (CAT) and superoxide dismutase (SOD) and malonedialdehyde (MDA). KCN significantly inhibited the activity of CCO, CAT and SOD, increased the level of p53, AChE and MDA as well as decreased the level of dopamine and serotonin. Early administration of trevo caused a reversal of all these biochemical at varying degree. Histological results showed that KCN had no observable effect on the morphology of the brain. Further work can be done on the effect of trevo on long-term exposure to KCN.

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

Background: Exposure to lead has been linked to biochemical changes similar to those patients suffering from Alzheimer’s disease. Trévo is a phytonutrient-rich product with antiaging and antioxidant properties. Purpose: To investigate the neuroprotective activity of trévo against lead-induced biochemical changes in male Wistar rats. Methods: The study involves 35 animals that were randomly divided into five groups of seven rats each. Group I (Control): Orally administered distilled water; Group II (Induced): Administered 15 mg/kg of lead acetate (PbA) intraperitoneally; Group III (Treatment group): Orally administered 2 mL/kg of trévo for two days before co-administration with PbA for 12 consecutive days; Group IV (Treatment group): Orally administered 5 mL/kg of trévo for two days prior to coadministration with PbA for 12 consecutive days; Group V: Orally administered 5 mL/kg of trévo for 14 consecutive days. Animals were anesthetized with diether and the brain excised and processed for the following biochemical assays: Malonedialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GT), acetylcholinesterase (AChE), beta-amyloid, glutamate, Na+/K+ ATPase, and glutamate dehydrogenase (GD). Results: PbA caused significant oxidative stress (increased MDA concentration, decreased GSH concentration, suppressed the activity of CAT, SOD), decreased GT activity, increased activity of AChE, increased the concentration of beta-amyloid, and caused glutamate excitotoxicity (increased concentration of glutamate, decreased activity of Na+/K+ ATPase, and GD) in rat brains. Treatment with trévo at the two different doses significantly prevented oxidative damage, beta-amyloid aggregation, glutamate excitotoxicity, and acetylcholine breakdown induced by lead acetate. Conclusion: Our findings added to the reported pharmacological activity of trévo and supported the antiaging potential of trévo.

Ethnopharmacological relevance Different parts of Antiaris africana Englea (Moraceae) are used traditionally for the treatment of various diseases, including epilepsy and other nervous system disorders. Aims of this study The current study was designed to evaluate the neuroprotective activity of flavonoids isolated from A. africana against potassium cyanide (KCN)-induced oxidative damage in brain homogenate. Materials and methods Dried and ground leaves of A. africana were extracted with methanol and fractioned into n-hexane (HFA), dichloromethane (DFA), ethyl acetate (EFA) and methanol (MFA). Each fraction was assessed for neuroprotective potential by anticholinesterase activity test. The fraction with the best anticholinesterase activity was subjected to various chromatographic techniques through bioassay-guided fractionation to isolate the bioactive compounds. The protective ability of the extract, fractions and compounds against Potassium cyanide (KCN)-induced mitochondrial damage in rat brain homogenate was evaluated. Structures of the isolated compounds were determined using 1D and 2D NMR, mass spectrometry and by comparison with literature data. Results and discussion The ethyl acetate fraction showed the best anticholinesterase activity with an IC50 of 23.23 ± 1.12 μg/ml. Quercetin and a biflavonoid glucoside identified as 3′-4′-bisquercetin-3β-D-diglucoside from this fraction displayed a remarkable antioxidant activity in the DPPH assay and showed significant (P Conclusion Quercetin and the bisquercetin-diglucoside isolated from the leaves of A. Africana for the first time, are major contributors to the observed neuroprotective property of the plant which supports its folkloric usage in the management of seizures, epilepsy and other neurological disorders.

Ischemia-reperfusion injury is a urological emergency condition that could lead to necrosis, testicular damage subfertility, and infertility. The purpose of this study was to identify changes taking place in the rat testis at short-term (4 hr) as well as long-term (7 days) reperfusion following testicular torsion and to evaluate the effects of Proxeed Plus (PP), L-carnitine-rich antioxidant supplement, on preventing these changes using the biochemical parameters and histopathology. Thirty adult male rats were divided into five groups: in groups, 1-4 testicular ischemia was achieved by rotating the left testis 720° clockwise for 4 h and dividing into the sham, torsion/detorsion (T/D), T/D+1000 mg/kg BW PP, and T/D+5000 mg/kg BW PP groups, respectively. PP was administered intraperitoneally 30 min before detorsion while group 5 served as the normal control. All rats were sacrificed 4 h after detorsion. The same experimental design was set up, and animals were sacrificed after 7 days of detorsion. The testicular levels of human cyclooxygenase-2; tumor necrosis factor; interleukins-1β, 6, and 10; hydrogen peroxide; malonaldehyde; superoxide dismutase; catalase; glutathione transferase; glutathione peroxidase; glutathione reductase; and histopathological damage were evaluated. Our results revealed that rats in the torsion/detorsion group exhibited elevated testicular levels of oxidative markers and proinflammatory cytokines, low levels of antioxidant enzymes, and severe histological alterations relative to the control and sham groups. Treatments with 1000 and 5000 mg/kg BW of PP for 4 hr and 7 days significantly ( p < 0.05 ) decreased the levels of the proinflammatory and oxidative markers while increasing the spermatogenesis, testicular levels of antioxidant enzymes, and anti-inflammatory cytokine (IL-10) in a dose-dependent manner. This suggested that PP exhibited anti-inflammatory and antioxidant activities against I/R testes thus serving as an effective supplement to protect against testicular assault.

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

Avermectins are a group of drugs that occurs naturally as a product of fermenting Streptomyces avermitilis, an actinomycetes, isolated from the soil. Eight different structures, including ivermectin, abamectin, doramectin, eprinomectin, moxidectin, and selamectin, were isolated and divided into four major components (A1a, A2a, B1a and B2a) and four minor components (A1b, A2b, B1b, and B2b). Avermectins are generally used as a pesticide for the treatment of pests and parasitic worms as a result of their anthelmintic and insecticidal properties. Additionally, they possess anticancer, anti-diabetic, antiviral, antifungal, and are used for treatment of several metabolic disorders. Avermectin generally works by preventing the transmission of electrical impulse in the muscle and nerves of invertebrates, by amplifying the glutamate effects on the invertebrates-specific gated chloride channel. Avermectin has unwanted effects or reactions, especially when administered indiscriminately, which include respiratory failure, hypotension, and coma. The current review examines the mechanism of actions, biosynthesis, safety, pharmacokinetics, biological toxicity and activities of avermectins.

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.

Simple Summary We used multi-omics approaches to evaluate the association of complement signature C3/C5/C3AR1/C5AR1 with tumor immune phenotypes and prognosis across various cancer types. We found that the gene signatures have deregulated expression in human malignancies and demonstrated context-dependent association with tumor immune evasion, prognosis, and therapy response across the various cancer types. Further analysis revealed that C3, C5, C3AR1, and C5AR1 were associated with tumor immune evasion via dysfunctional T-cell phenotypes with a lesser contribution of T-cell exclusion. Lastly, we also demonstrated that the expression levels of C3, C5, C3AR1, and C5AR1 were associated with context-dependent chemotherapy, lymphocyte-mediated tumor killing, and immunotherapy outcomes in different cancer types. The complement components C3, C5, C3AR1, and C5AR1 serve as attractive targets for strategizing cancer immunotherapy and response follow-up. Abstract Despite the advances in our understanding of the genetic and immunological basis of cancer, cancer remains a major public health burden with an ever-increasing incidence rate globally. Nevertheless, increasing evidence suggests that the components of the complement system could regulate the tumor microenvironment (TME) to promote cancer progression, recurrence, and metastasis. In the present study, we used an integrative multi-omics analysis of clinical data to explore the relationships between the expression levels of and genetic and epigenetic alterations in C3, C5, C3AR1, and C5AR1 and tumor immune evasion, therapy response, and patient prognosis in various cancer types. We found that the complements C3, C5, C3AR1, and C5AR1 have deregulated expression in human malignancies and are associated with activation of immune-related oncogenic processes and poor prognosis of cancer patients. Furthermore, we found that the increased expression levels of C3, C5, C3AR1, and C5AR1 were primarily predicted by copy number variation and gene methylation and were associated with dysfunctional T-cell phenotypes. Single nucleotide variation in the gene signature co-occurred with multiple oncogenic mutations and is associated with the progression of onco-immune-related diseases. Further correlation analysis revealed that C3, C5, C3AR1, and C5AR1 were associated with tumor immune evasion via dysfunctional T-cell phenotypes with a lesser contribution of T-cell exclusion. Lastly, we also demonstrated that the expression levels of C3, C5, C3AR1, and C5AR1 were associated with context-dependent chemotherapy, lymphocyte-mediated tumor killing, and immunotherapy outcomes in different cancer types. In conclusion, the complement components C3, C5, C3AR1, and C5AR1 serve as attractive targets for strategizing cancer immunotherapy and response follow-up.

Background: Oxidative stress plays a significant role in stroke pathogenesis. Hence, plants rich in antioxidant phytochemicals have been suggested as effective remedies for prevention and treatment of stroke and other neurological diseases. Antiaris africana Engl. (Moraceae) is traditionally used for the management of brain-related problems but there is paucity of data on its anti-stroke potential. Materials and Methods: Ischemia/reperfusion injury was induced by a 30 min bilateral common carotid artery occlusion/ 2 h reperfusion (BCCAO/R) in the brain of male Wistar rats. A sham-operated group which was not subjected to BCCAO/R and a group subjected to BCCAO/R without treatment with MEA served as controls. The ameliorative effect of 14 days of pretreatment with 50 mg/kg or 100 mg/kg A. africana methanol leaf extract (MEA) on BCCAO/R-mediated alterations to key markers of oxidative stress (malondialdehyde, reduced glutathione, xanthine oxidase, superoxide dismutase, catalase and glutathione peroxidase) and neurochemical disturbances and excitotoxicity (myeloperoxidase, glutamine synthetase, Na+/K+ ATPase, acetylcholinesterase and tyrosine hydroxylase), was evaluated and compared with the effect produced by treatment with 20 mg/kg quercetin as a reference standard. Results: Results show that pretreatment with MEA significantly mitigated or reversed BCCAO/R-induced changes in the level or activity of the evaluated biochemical markers of oxidative stress, neurochemical dysfunction and excitotoxicity compared with the BCCAO/R untreated control group (p < 0.05). The effect produced by 100 mg/kg MEA was similar to that of the reference standard, quercetin. Conclusion: These results revealed the neuroprotective potential of A. africana in stroke and other ischemia-related pathologies. Key words: brain ischemia

The increasing popularity of herbal medicine and the well-established health benefits of phytochemicals have spurred the multiplicity of nutraceutical and phytopharmaceutical products. In this study, TrévoTM, a nutraceutical and phytopharmaceutical product, was evaluated for beneficial effects in acetaminophen-induced hepatic toxicity in Wistar rats. Animals received TrévoTM (1.5 mL/kg, 3.0 mL/kg or 4.5 mL/kg) orally for 14 days. Hepatotoxicity wasinduced by the oral administration of acetaminophen (2 g/kg), 24 h priorto sacrifice.Biochemical liverfunction tests, oxidative stress indicators and histoarchitectural changes were evaluated. Acetaminophen administration occasioned significant increase (P < 0.05) in serum bilirubin level and activities ofthe aminotransferases, alkaline phosphatase, -glutamyltransferase and lactate dehydrogenase accompanied by a significant decrease (P < 0.05) in albumin level as well as histopathological alterations in liver sections. Promotion of hepatic oxidative stress by acetaminophen wasrevealed by significant (P < 0.05) increase in lipid peroxidation, depletion of reduced glutathione, and decrease in superoxide dismutase and catalase activities. Administration of TrévoTM remarkably ameliorated acetaminophen-induced histopathological alterations and changes in serum and tissue biochemical markers. The protective effect of TrévoTM (4.5 mL/kg) was at par with that of Silymarin (25 mg/kg). The present study indicates that TrévoTM has notable salubrious effects.

Background The physiopathologies of many neurologic diseases are characterized by related biochemical dysfunctions that could be explored as drug targets. This study evaluated the effect of a methanol leaf extract of Antiaris africana (MEA) on critical bioindices of Parkinsonism and related neurologic dysfunctions in rats with rotenone-induced neurotoxicity. Methods Animals were administered 50 or 100 mg/kg MEA for 14 consecutive days. Rotenone (1.5 mg/kg) was administered three times per day on days 13 and 14. Coenzyme Q10 (5 mg/kg) was the reference drug. Complex I activity, dopamine level, activities of acetylcholinesterase, myeloperoxidase, Na+/K+ ATPase and glutamine synthetase, as well as oxidative stress indices were evaluated at the end of the period of treatment. Results Rotenone-intoxicated group showed disruption of complex 1 activity, dopamine level, and glutamine synthetase activity with negative alterations to activities of acetylcholinesterase, myeloperoxidase, and Na+/K+ ATPase as well as heightened cerebral oxidative stress. MEA restored brain mitochondria functionality, mitigated altered neurochemical integrity, and ameliorated cerebral oxidative stress occasioned by rotenone neurotoxicity. The activity of A. Africana was comparable with that of 5 mg/kg coenzyme Q10. Conclusions These results indicated that A. africana displayed therapeutic potential against Parkinsonism and related neurologic dysfunctions and support its ethnobotanical use for the treatment of neurologic disorders.

The study was aimed at evaluating the toxicological and antioxidant activities of Antiaris africana Engl. (family Moraceae), that is used in Nigeria and other West Africa countries as a panacea for the treatment of several ailments. The methanolic extract of A. africana (MEA) obtained was analysed for antioxidant activities in vitro and screened for various phytochemicals present. Phenolic and flavonoid contents were determined followed with high performance liquid chromatography -diode-array detection (HPLC-DAD) fingerprinting of phenolic content. Furthermore, the sub-acute toxicity of MEA was determined via oral administration of varying doses for 14 consecutive days (0, 50, 100, 200 and 400 mg/kg) in rats. After oral administration for 14 consecutive days in male rats, the toxicity effect was assayed by determining aspartate aminotransferase (AST) and alanine aminotransferase (ALT) for hepatic function; urea and creatinine for renal function; creatinine kinase (CK) for cardiac function; and lipid profile. HPLC results showed that the major phenolics present are quercetin, rutin, caffeic acid, garlic acid and quercetin. MEA was able to scavenge diphenyl picryl hydrazyl, hydroxyl and nitric oxide radicals and prevent lipid peroxidation induced by ferrous sulphate at all concentration tested. The toxicology investigation showed that at low doses, A. africana is non-toxic, while at high doses; it is moderately toxic to the animals. In conclusion, A. Africana is generally non-toxic; however, care must be taken in administration at higher doses. Key words: Toxicology, HPLC, phytochemicals, Antiaris africana.

Background In the past few years, there has been a tremendous increase in the number of plant-based health supplements with respect to their safety and efficacy in diseases treatment and prevention. Solanum dasyphyllum, also known as Africa eggplant is ethnomedicinally used as an antivenom, pain reliever and anticonvulsant in various part of Nigeria, however, there is no scientific data to support some of these claims. Methods This study evaluated the protective effect of solvent fractions of Solanum dasyphyllum, hexane fraction of S. dasyphyllum (HFSD), dichloromethane fraction of S. dasyphyllum (DFSD), ethylacetate fraction of S. dasyphyllum (EAFSD), methanolic fraction of S. dasyphyllum (MFSD) and crude fraction of S. dasyphyllum (CFSD) on cyanide-induced oxidative stress and neurotoxicity in vitro in the cerebral cortex. Neuroprotective activities were evaluated by assaying for markers of oxidative stress, neurotoxicity and electron transport system enzymes via evaluating lipid peroxidation (LPO), protein carbonyl (PC), reduced glutathione (GSH), acetylcholinesterase (AChE), NADH-succinate dehydrogenase (NSD), NADH-cytochrome c reductase (NCR), and succinate-cytochrome c reductase (SCR) in the homogenate of cerebral cortex. Results The results showed that all solvent fractions of S. dasyphyllum significantly ameliorated cyanide-induced oxidative stress (P

Background: Oxidative stress plays a significant role in stroke pathogenesis. Hence, plants rich in antioxidant phytochemicals have been suggested as effective remedies for prevention and treatment of stroke and other neurological diseases. Antiaris africana Engl. (Moraceae) is traditionally used for the management of brain-related problems but there is paucity of data on its anti-stroke potential. Materials and Methods: Ischemia/reperfusion injury was induced by a 30 min bilateral common carotid artery occlusion/ 2 h reperfusion (BCCAO/R) in the brain of male Wistar rats. A sham-operated group which was not subjected to BCCAO/R and a group subjected to BCCAO/R without treatment with MEA served as controls. The ameliorative effect of 14 days of pretreatment with 50 mg/kg or 100 mg/kg A. africana methanol leaf extract (MEA) on BCCAO/R-mediated alterations to key markers of oxidative stress (malondialdehyde, reduced glutathione, xanthine oxidase, superoxide dismutase, catalase and glutathione peroxidase) and neurochemical disturbances and excitotoxicity (myeloperoxidase, glutamine synthetase, Na+/K+ ATPase, acetylcholinesterase and tyrosine hydroxylase), was evaluated and compared with the effect produced by treatment with 20 mg/kg quercetin as a reference standard. Results: Results show that pretreatment with MEA significantly mitigated or reversed BCCAO/R-induced changes in the level or activity of the evaluated biochemical markers of oxidative stress, neurochemical dysfunction and excitotoxicity compared with the BCCAO/R untreated control group (p < 0.05). The effect produced by 100 mg/kg MEA was similar to that of the reference standard, quercetin. Conclusion: These results revealed the neuroprotective potential of A. africana in stroke and other ischemia-related pathologies.