8 research outputs found
HPLC quantification of phenolic content and assessment of methanolic extract of Antiaris africana for toxicological study
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.Keywords: Toxicology, HPLC, phytochemicals, Antiaris african
MODULATION OF KEY BIOCHEMICAL MARKERS RELEVANT TO STROKE BY ANTIARIS AFRICANA LEAF EXTRACT FOLLOWING CEREBRAL ISCHEMIA/REPERFUSION INJURY
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
a-Amylase inhibition, anti-glycation property and characterization of the binding interaction of citric acid with a-amylase using multiple spectroscopic, kinetics and molecular docking approaches
The quest to suppress complications associated with diabetes mellitus is ever increasing, while food additives
and preservatives are currently being considered to play additional roles besides their uses in food
enhancement and preservation. In the present study, the protective prowess of a common food preservative
(citric acid, CA) against advanced glycation end-products (AGEs) formation and its binding interaction
mechanism with a-amylase (AMY), an enzyme linked with hyperglycemia management, were
examined. Enzyme inhibition kinetics, intrinsic fluorescence, synchronous and 3D fluorescence spectroscopies,
ultraviolet–visible (UV–Vis) absorption spectroscopy, Fourier transform-infrared (FT-IR) spectroscopy,
thermodynamics, and molecular docking analyses were employed. Results obtained showed
that citric acid decreased a-amylase activity via mixed inhibition (IC50 = 5.01 ± 0.87 mM,
Kic = 2.42 mM, Kiu = 160.34 mM) and suppressed AGEs formation (IC50 = 0.795 ± 0.001 mM). The intrinsic
fluorescence of free a-amylase was quenched via static mechanism with high bimolecular quenching
constant (Kq) and binding constant (Ka) values. Analysis of thermodynamic properties revealed that
AMY-CA complex was spontaneously formed (DG DH), with involvement
of electrostatic forces. UV–Vis, FT-IR and 3D fluorescence spectroscopies affirmed alterations in aamylase
native conformation due to CA binding interaction. CA interacted with His-101, Asp-197, His-
299, and Glu-233 within AMY active site. Our findings indicated that CA could impair formation of
AGEs and interact with a-amylase to slow down starch hydrolysis; vital properties in management of
type 2 diabetes complications
Neuromodulatory effect of solvent fractions of Africa eggplant (Solanium dadyphyllum) against KCN-induced mitochondria damage, viz. NADH-succinate dehydrogenase, NADH- cytochrome c reductase, and succinate-cytochrome c reductase
Abstract 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 < 0.05). It inhibited the activity of acetylcholinesterase-HFSD (68.42 ± 5.37%), DFSD (36.32 ± 5.45%), EFA (20 ± 0.69%), MFSD (33.16 ± 4.8%) and CFSD (35.79 ± 2.8%), increased the activity of NSD [HFSD (94.74 ± 7.3%), EAFSD (78.95 ± 5.4%) and CFSD (60.53 ± 4.6%)], while DFSD (− 5.26 ± 1.4%) and MFSD (− 7.9 ± 0.4%) had a negative effect, increased the activity of NCR [HFSD (91.89 ± 7.1%), DFSD (90.54 ± 8.2%), EAFSD (62.16 ± 4.7%); MFSD (306.76 ± 7.2%) and CFSD (154.0 ± 8.1%)]. All the solvent fractions also significantly increased the activity of SCR [HFSD (70.59 ± 3.8%), EAFSD (58.82 ± 6.4%), MFSD (88.24 ± 9.0%) CFSD (76.47 ± 8.2%)] apart from DFSD (− 5.88 ± 1.2%) in rat cerebral cortex. Conclusion This result shows that S. dasyphyllum has neuroprotective activities, however HFSD shows the most potent bioactivities in maintaining mitochondria integrity by preserving the electron transport system. Further work can be done on isolating and characterizing the bioactive compound in HFSD for novel natural product in the treatment of neurological disorders
Reversal effect of Solanum dasyphyllum against rotenone-induced neurotoxicity
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
Reversal of acetaminophen-generated oxidative stress and concomitant hepatotoxicity by a phytopharmaceutical product
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
Avermectin Derivatives, Pharmacokinetics, Therapeutic and Toxic Dosages, Mechanism of Action, and Their Biological Effects
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