Neuromodulatory effects of ethyl acetate fraction of Zingiber of?cinale Roscoe extract in rats with lead-induced oxidative stress
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摘要
Objective: This study investigated the ameliorative potential of Zingiber officinale Roscoe extract against lead-induced brain damage in rats.Methods: Thirty male rats were divided into 5 groups of 6 rats each. Lead-acetate toxicity was induced by intraperitoneal injection(10 mg/kg body weight(b.w.)) in Groups B–E. Group A(control) and Group B(lead-acetate) were left untreated; vitamin C(200 mg/kg b.w.) was administered to Group C; ethyl acetate fraction from Z. officinale extract(200 and 100 mg/kg b.w.) was administered to Group D and E by oral gavage once daily for 7 days. Changes in the content of some key marker enzymes such as acetylcholinesterase(AChE), butyrylcholinesterase(BChE), monoamine oxidase(MAO), epinephrine, dopamine,Na~+/K~+-ATPase, catalase(CAT), superoxide dismutase(SOD) and glutathione peroxidase(GPx) as well as malonaldehyde(MDA) levels were determined in serum.Results: Exposure to lead acetate resulted in a significant decrease(P < 0.05) in the activities of BChE,AChE, Na~+/K~+-ATPase, SOD, CAT and GPx with a corresponding increase in the levels of MDA, xanthine oxidase, epinephrine, dopamine and MAO relative to the control group. Levels of all disrupted parameters were alleviated by co-administration of Z. officinale fraction and by the standard drug, vitamin C.Conclusion: These results suggest that ethyl acetate fraction of Z. officinale extract attenuates leadinduced brain damage and might have therapeutic potential as a supplement that can be applied in lead poisoning.
Objective: This study investigated the ameliorative potential of Zingiber officinale Roscoe extract against lead-induced brain damage in rats.Methods: Thirty male rats were divided into 5 groups of 6 rats each. Lead-acetate toxicity was induced by intraperitoneal injection(10 mg/kg body weight(b.w.)) in Groups B–E. Group A(control) and Group B(lead-acetate) were left untreated; vitamin C(200 mg/kg b.w.) was administered to Group C; ethyl acetate fraction from Z. officinale extract(200 and 100 mg/kg b.w.) was administered to Group D and E by oral gavage once daily for 7 days. Changes in the content of some key marker enzymes such as acetylcholinesterase(AChE), butyrylcholinesterase(BChE), monoamine oxidase(MAO), epinephrine, dopamine,Na~+/K~+-ATPase, catalase(CAT), superoxide dismutase(SOD) and glutathione peroxidase(GPx) as well as malonaldehyde(MDA) levels were determined in serum.Results: Exposure to lead acetate resulted in a significant decrease(P < 0.05) in the activities of BChE,AChE, Na~+/K~+-ATPase, SOD, CAT and GPx with a corresponding increase in the levels of MDA, xanthine oxidase, epinephrine, dopamine and MAO relative to the control group. Levels of all disrupted parameters were alleviated by co-administration of Z. officinale fraction and by the standard drug, vitamin C.Conclusion: These results suggest that ethyl acetate fraction of Z. officinale extract attenuates leadinduced brain damage and might have therapeutic potential as a supplement that can be applied in lead poisoning.
Objective: This study investigated the ameliorative potential of Zingiber officinale Roscoe extract against lead-induced brain damage in rats.Methods: Thirty male rats were divided into 5 groups of 6 rats each. Lead-acetate toxicity was induced by intraperitoneal injection(10 mg/kg body weight(b.w.)) in Groups B–E. Group A(control) and Group B(lead-acetate) were left untreated; vitamin C(200 mg/kg b.w.) was administered to Group C; ethyl acetate fraction from Z. officinale extract(200 and 100 mg/kg b.w.) was administered to Group D and E by oral gavage once daily for 7 days. Changes in the content of some key marker enzymes such as acetylcholinesterase(AChE), butyrylcholinesterase(BChE), monoamine oxidase(MAO), epinephrine, dopamine,Na~+/K~+-ATPase, catalase(CAT), superoxide dismutase(SOD) and glutathione peroxidase(GPx) as well as malonaldehyde(MDA) levels were determined in serum.Results: Exposure to lead acetate resulted in a significant decrease(P < 0.05) in the activities of BChE,AChE, Na~+/K~+-ATPase, SOD, CAT and GPx with a corresponding increase in the levels of MDA, xanthine oxidase, epinephrine, dopamine and MAO relative to the control group. Levels of all disrupted parameters were alleviated by co-administration of Z. officinale fraction and by the standard drug, vitamin C.Conclusion: These results suggest that ethyl acetate fraction of Z. officinale extract attenuates leadinduced brain damage and might have therapeutic potential as a supplement that can be applied in lead poisoning.
引文
[1] Mathew BB, Tiwari A, Jatawa SK. Free radicals and antioxidants:a review. J Pharm Res 2011;4(12):4340–3.
[2] Gurer H, Ercal N. Can antioxidant be beneficial in the treatment of lead poisoning? Free Radic Biol Med 2000;29(10):927–45.
[3] Dart RC, Hurlbut KM, Boyer-Hassen LV. Medical Toxicology. 3rd ed. Philadelphia:Lippincott Williams&Wilkins; 2004. p. 1423–31.
[4] Bellinger DC. Lead. Pediatr 2004;113(4 Suppl):1016–22.
[5] Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M, Egelhoff JC, et al.Decreased brain volume in adults with childhood lead exposure. PLoS Med2008;5(5):e112.
[6] Needleman H. Low level lead exposure:history and discovery. Am Epidemiol2009;19:235–8.
[7] Guilarte TR. Glutamatergic system and developmental lead neurotoxicity.Neurotoxicol 1997;18:665–72.
[8] White LD, Cory-Slechta DA, Gilbert ME, Tiffany-Castiglioni E, Zawia NH,Virgolini M, et al. New and evolving concepts in the neurotoxicology of lead.Toxicol Appl Pharmacol 2007;225(1):1–27.
[9] Ozawa S, Kamiya H, Tsuzuki K. Glutamate receptors in the mammalian central nervous system. Prog Neurobiol 1998;54:581–618.
[10] Nihei MK, Guilarte TR. Molecular changes in glutamatergic synapses induced by Pb2+:association with deficits in LTP and spatial learning. Neurotoxicology2001;22(5):635–43.
[11] Ojo OA, Ojo AB, Osukoya OA, Ajiboye BO. Aqueous Extract of Carica papaya Linn roots halts sodium arsenite-induced renal inflammation through inhibiting adenosine deaminase, 8-hydroxy-2’-deoxyguanosine, C-reactive protein and inducible nitric oxide synthase activity. Serbian J Exp Clin Res 2017;18(4):323–30.
[12] World Health Organization. WHO Guidelines on Safety Monitoring of Herbal Medicines in Pharmacovigilance Systems. Geneva, Switzerland:World Health Organization; 2004.
[13] Aggarwal BB, Shishodia S. Molecular targets of dietary agents for prevention and therapy of cancer. Biochem Pharmacol 2006;71(10):1397–421.
[14] Chan SJ, San Segundo B, McCormick MB, Steiner DF. Nucleotide and predicted amino acid sequences of cloned human and mouse preprocathepsin B c DNAs.Proc Natl Acad Sci U S A 1986;83(20):7721–5.
[15] Asfaw N, Abegaz B. Chemical constituents of the essential oils of Zingiber of?cinale Roscoe cultivated in Ethiopia. SINET Ethiop J Sci 1995;18:133–5.
[16] Zancan KC, Marques MMO, Petenate AJ, Miereles MAA. Extraction of ginger oleoresin with coz and co-solvents:a study of antioxidant action of the extracts. J Supercit Flu 2002;24:57–76.
[17] Khaki AA, Khaki A. Antioxidant effect of ginger to prevent lead-induced liver tissue apoptosis in rat. J Med Plants Res 2010;4:1492–5.
[18] Mentreddy SR. Medicinal plant species with potential antidiabetic properties. J Sci Food Agric 2007;87:743–50.
[19] Ippoushi K, Azuma K, Ito H, Horie H, Higashio H. 6-Gingerol inhibits nitric oxide synthesis in activated J774.1 mouse macrophages and prevents peroxynitrite-induced oxidation and nitration reactions. Life Sci 2003;73(26):3427–37.
[20] Jagetia GC, Baliga MS, Venkatesh P, Ulloor JN. Influence of ginger rhizome(Zingiber of?cinale Rosc)on survival, glutathione and lipid peroxidation in mice after whole-body exposure to c radiation. Radiat Res 2003;160(5):584–92.
[21] Meyer JH, Ginovart N, Boovariwala A, Sagrati S, Hussey D, Garcia A, et al.Elevated monoamine oxidase A levels in the brain:an explanation for the monoamine imbalance of major depression. Arch Gen Psychiatry 2006;63(11):1209–16.
[22] Wuwongse S, Chang RC, Law AC. The putative neurodegenerative links between depression and Alzheimer’s disease. Progr Neurobiol 2010;91:362–75.
[23] Ojo OA, Ojo AB, Ajiboye BO, Oyinloye BE, Akinyemi AJ, Okesola MA, et al.Chromatographic fingerprint analysis, antioxidant properties, and inhibition of cholinergic enzymes(acetylcholinesterase and butyrylcholinesterase)of phenolic extracts from Irvingia gabonensis(Aubry-Lecomte ex O’Rorke)Baill bark. J Basic Clin Physiol Pharmacol 2018;29(2):217–24.
[24] Ardan T, Kovaceva J, CejkováJ. Comparative histochemical and immunohistochemical study on xanthine oxidoreductase/xanthine oxidase in mammalian corneal epithelium. Acta Histochem 2004;106(1):69–75.
[25] Ojo OA, Ojo AB, Awoyinka O, Ajiboye BO, Oyinloye BE, Osukoya OA, et al.Aqueous extract of Carica papaya Linn roots potentially attenuates arsenic induced biochemical and genotoxic effects in Wistar rats. J Trad Compl Med2018;8(2):324–34.
[26] Ojo OA, Ojo AB, Ajiboye BO, Olaiya O, Akawa A, Olaoye O, et al. Inhibitory effect of Bryophyllum pinnatum(Lam.)Oken leaf extract and their fractions on aamylase, a-glucosidase and cholinesterase enzyme. Pharmacog J 2018;10(3):497–506.
[27] Reddy YA, Chalamaiah M, Ramesh B, Balaji G, Indira P. Ameliorating activity of ginger(Zingiber of?cinale)extract against lead induced renal toxicity in male rats. J Food Sci Technol 2014;51(5):908–14.
[28] Stephan JS, Fioriti L, Lamba N, Colnaghi L, Karl K, Derkatch IL, et al. The CPEB3protein is a functional prion that interacts with actin cytoskeleton. Cell Rep2015;11(11):1772–85.
[29] Ellman GL, Courtney KD, Andres V, Featherstone RM. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol 1961;7:88–95.
[30] Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1979;95(2):351–8.
[31] Turski WA, Cavalheiro EA, Schwarz M, Czuczwar SJ, Kleinrok Z, Turski L. Limbic seizures produced by pilocarpine in rats:behavioural, electroencephalographic and neuropathological study. Behav Brain Res 1983;9(3):315–35.
[32] Wyse AT, Streck EL, Barros SV, Brusque AM, Zugno AI, Wajner M.Methylmalonate administration decreases Na+/K+-ATPase activity in cerebral cortex of rats. NeuroReport 2000;11(10):2331–4.
[33] Peuler JD, Johnson GA. Simultaneous single isotope radioenzymatic assay of plasma norepinephrine, epinephrine and dopamine. Life Sci 1997;21:625–36.
[34] Marcocci L, Packer L, Droy-Lefaix MT, Sekaki A, Gardès-Albert M. Antioxidant action of Ginkgo biloba extract EGb 761. Methods Enzymol 1994;234:462–75.
[35] Misra HP, Fridovich I. The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem1972;247(10):3170–5.
[36] Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121–6.
[37] Flohe L, Gunzler WA. Assays of glutathione peroxidase. Methods Enzymol1984;105:114–21.
[38] Ali BH, Blunden G, Tanira MO, Nemmar A. Some phytochemical,pharmacological and toxicological properties of ginger(Zingiber of?cinale Roscoe):a review of recent research. Food Chem Toxicol 2008;46:409–20.
[39] Bay?r H, Kochanek PM, Kagan VE. Oxidative stress in immature brain after traumatic brain injury. Dev Neurosci 2006;28(4–5):420–31.
[40] Ojo OA, Ajiboye BO, Ojo AB, Olayide I, Akinyemi AJ, Fadaka AO, et al. HPLC-DAD fingerprinting analysis, antioxidant activity of phenolic extracts from Blighia sapida bark and its inhibition of cholinergic enzymes linked to Alzheimer’s disease. Jordan J Biol Sci 2017;10(4):257–64.
[41] Ademosun AO, Oboh G. Comparison of the inhibition of monoamine oxidase and butyrylcholinesterase activities by infusions from green tea and some citrus peels. Int J Alzheimers Dis 2014;2014:586407.
[42] Greig NH, Utsuki T, Yu Q, Zhu X, Holloway HW, Perry T, et al. A new therapeutic target in Alzheimer’s disease treatment:attention to butyrylcholinesterase. Curr Med Res Opin 2001;17(3):159–65.
[43] Wang J, Yang Z, Liu L, Zhao Z, Liu Z, Liu X. Protective effect of naringenin against lead-induced oxidative stress in rats. Biol Trace Elem Res 2012;146(3):354–9.
[44] Abdel-Wahhab M, Aly S. Antioxidant property of Nigella sativa(black cumin)and Syzygium aromaticum(clove)in rats during aflatoxicosis. J Appl Toxicol2005;25(3):218–23.
[45] El-Nekeety AA, El-Kady AA, Soliman MS, Hassan NS, Abdel-Wahhab MA.Protective effect of Aquilegia vulgaris(L.)against lead acetate-induced oxidative stress in rats. Food Chem Toxicol 2009;47(9):2209–15.
[46] Ajiboye BO, Akalabu MC, Ojo OA, Afolabi OB, Okesola MA, Olayide I, et al.Inhibitory effect of ethyl acetate fraction of Solanum macrocarpon L. leaves on cholinergic, monoaminergic, and purinergic enzyme activities. J Food Biochem2018;42(6):e12643.
[47] Randrup A, Munkvad I, Pog R. Mania, depression, and brain dopamine. In:Essman W, Valzelli L, editors. Current Developments in Psychopharmacology. New York:Spectrum Publications; 1975. p. 206–48.
[48] Ajiboye BO, Ojo OA, Okesola MA, Oyinloye BE, Kappo AP. Ethyl acetate leaf fraction of Cnidoscolus aconitifolius(Mill.)I. M. Johnst:antioxidant potential,inhibitory activities of key enzymes on carbohydrate metabolism, cholinergic,monoaminergic, purinergic and chemical fingerprinting. Int J Food Prop2018;21(1):1697–715.
[49] Boots AW, Haenen GR, Bast A. Health effects of quercetin:from antioxidant to nutraceutical. Eur J Pharmacol 2008;585:325–37.
[50] Ojo OA, Ajiboye BO, Oyinloye BE, Ojo AB, Olarewaju OI. Protective effect of Irvingia gabonensis stem bark extract on cadmium-induced nephrotoxicity in rats. Interdiscip Toxicol 2014;7(4):208–14.
[2] Gurer H, Ercal N. Can antioxidant be beneficial in the treatment of lead poisoning? Free Radic Biol Med 2000;29(10):927–45.
[3] Dart RC, Hurlbut KM, Boyer-Hassen LV. Medical Toxicology. 3rd ed. Philadelphia:Lippincott Williams&Wilkins; 2004. p. 1423–31.
[4] Bellinger DC. Lead. Pediatr 2004;113(4 Suppl):1016–22.
[5] Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M, Egelhoff JC, et al.Decreased brain volume in adults with childhood lead exposure. PLoS Med2008;5(5):e112.
[6] Needleman H. Low level lead exposure:history and discovery. Am Epidemiol2009;19:235–8.
[7] Guilarte TR. Glutamatergic system and developmental lead neurotoxicity.Neurotoxicol 1997;18:665–72.
[8] White LD, Cory-Slechta DA, Gilbert ME, Tiffany-Castiglioni E, Zawia NH,Virgolini M, et al. New and evolving concepts in the neurotoxicology of lead.Toxicol Appl Pharmacol 2007;225(1):1–27.
[9] Ozawa S, Kamiya H, Tsuzuki K. Glutamate receptors in the mammalian central nervous system. Prog Neurobiol 1998;54:581–618.
[10] Nihei MK, Guilarte TR. Molecular changes in glutamatergic synapses induced by Pb2+:association with deficits in LTP and spatial learning. Neurotoxicology2001;22(5):635–43.
[11] Ojo OA, Ojo AB, Osukoya OA, Ajiboye BO. Aqueous Extract of Carica papaya Linn roots halts sodium arsenite-induced renal inflammation through inhibiting adenosine deaminase, 8-hydroxy-2’-deoxyguanosine, C-reactive protein and inducible nitric oxide synthase activity. Serbian J Exp Clin Res 2017;18(4):323–30.
[12] World Health Organization. WHO Guidelines on Safety Monitoring of Herbal Medicines in Pharmacovigilance Systems. Geneva, Switzerland:World Health Organization; 2004.
[13] Aggarwal BB, Shishodia S. Molecular targets of dietary agents for prevention and therapy of cancer. Biochem Pharmacol 2006;71(10):1397–421.
[14] Chan SJ, San Segundo B, McCormick MB, Steiner DF. Nucleotide and predicted amino acid sequences of cloned human and mouse preprocathepsin B c DNAs.Proc Natl Acad Sci U S A 1986;83(20):7721–5.
[15] Asfaw N, Abegaz B. Chemical constituents of the essential oils of Zingiber of?cinale Roscoe cultivated in Ethiopia. SINET Ethiop J Sci 1995;18:133–5.
[16] Zancan KC, Marques MMO, Petenate AJ, Miereles MAA. Extraction of ginger oleoresin with coz and co-solvents:a study of antioxidant action of the extracts. J Supercit Flu 2002;24:57–76.
[17] Khaki AA, Khaki A. Antioxidant effect of ginger to prevent lead-induced liver tissue apoptosis in rat. J Med Plants Res 2010;4:1492–5.
[18] Mentreddy SR. Medicinal plant species with potential antidiabetic properties. J Sci Food Agric 2007;87:743–50.
[19] Ippoushi K, Azuma K, Ito H, Horie H, Higashio H. 6-Gingerol inhibits nitric oxide synthesis in activated J774.1 mouse macrophages and prevents peroxynitrite-induced oxidation and nitration reactions. Life Sci 2003;73(26):3427–37.
[20] Jagetia GC, Baliga MS, Venkatesh P, Ulloor JN. Influence of ginger rhizome(Zingiber of?cinale Rosc)on survival, glutathione and lipid peroxidation in mice after whole-body exposure to c radiation. Radiat Res 2003;160(5):584–92.
[21] Meyer JH, Ginovart N, Boovariwala A, Sagrati S, Hussey D, Garcia A, et al.Elevated monoamine oxidase A levels in the brain:an explanation for the monoamine imbalance of major depression. Arch Gen Psychiatry 2006;63(11):1209–16.
[22] Wuwongse S, Chang RC, Law AC. The putative neurodegenerative links between depression and Alzheimer’s disease. Progr Neurobiol 2010;91:362–75.
[23] Ojo OA, Ojo AB, Ajiboye BO, Oyinloye BE, Akinyemi AJ, Okesola MA, et al.Chromatographic fingerprint analysis, antioxidant properties, and inhibition of cholinergic enzymes(acetylcholinesterase and butyrylcholinesterase)of phenolic extracts from Irvingia gabonensis(Aubry-Lecomte ex O’Rorke)Baill bark. J Basic Clin Physiol Pharmacol 2018;29(2):217–24.
[24] Ardan T, Kovaceva J, CejkováJ. Comparative histochemical and immunohistochemical study on xanthine oxidoreductase/xanthine oxidase in mammalian corneal epithelium. Acta Histochem 2004;106(1):69–75.
[25] Ojo OA, Ojo AB, Awoyinka O, Ajiboye BO, Oyinloye BE, Osukoya OA, et al.Aqueous extract of Carica papaya Linn roots potentially attenuates arsenic induced biochemical and genotoxic effects in Wistar rats. J Trad Compl Med2018;8(2):324–34.
[26] Ojo OA, Ojo AB, Ajiboye BO, Olaiya O, Akawa A, Olaoye O, et al. Inhibitory effect of Bryophyllum pinnatum(Lam.)Oken leaf extract and their fractions on aamylase, a-glucosidase and cholinesterase enzyme. Pharmacog J 2018;10(3):497–506.
[27] Reddy YA, Chalamaiah M, Ramesh B, Balaji G, Indira P. Ameliorating activity of ginger(Zingiber of?cinale)extract against lead induced renal toxicity in male rats. J Food Sci Technol 2014;51(5):908–14.
[28] Stephan JS, Fioriti L, Lamba N, Colnaghi L, Karl K, Derkatch IL, et al. The CPEB3protein is a functional prion that interacts with actin cytoskeleton. Cell Rep2015;11(11):1772–85.
[29] Ellman GL, Courtney KD, Andres V, Featherstone RM. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol 1961;7:88–95.
[30] Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1979;95(2):351–8.
[31] Turski WA, Cavalheiro EA, Schwarz M, Czuczwar SJ, Kleinrok Z, Turski L. Limbic seizures produced by pilocarpine in rats:behavioural, electroencephalographic and neuropathological study. Behav Brain Res 1983;9(3):315–35.
[32] Wyse AT, Streck EL, Barros SV, Brusque AM, Zugno AI, Wajner M.Methylmalonate administration decreases Na+/K+-ATPase activity in cerebral cortex of rats. NeuroReport 2000;11(10):2331–4.
[33] Peuler JD, Johnson GA. Simultaneous single isotope radioenzymatic assay of plasma norepinephrine, epinephrine and dopamine. Life Sci 1997;21:625–36.
[34] Marcocci L, Packer L, Droy-Lefaix MT, Sekaki A, Gardès-Albert M. Antioxidant action of Ginkgo biloba extract EGb 761. Methods Enzymol 1994;234:462–75.
[35] Misra HP, Fridovich I. The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem1972;247(10):3170–5.
[36] Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121–6.
[37] Flohe L, Gunzler WA. Assays of glutathione peroxidase. Methods Enzymol1984;105:114–21.
[38] Ali BH, Blunden G, Tanira MO, Nemmar A. Some phytochemical,pharmacological and toxicological properties of ginger(Zingiber of?cinale Roscoe):a review of recent research. Food Chem Toxicol 2008;46:409–20.
[39] Bay?r H, Kochanek PM, Kagan VE. Oxidative stress in immature brain after traumatic brain injury. Dev Neurosci 2006;28(4–5):420–31.
[40] Ojo OA, Ajiboye BO, Ojo AB, Olayide I, Akinyemi AJ, Fadaka AO, et al. HPLC-DAD fingerprinting analysis, antioxidant activity of phenolic extracts from Blighia sapida bark and its inhibition of cholinergic enzymes linked to Alzheimer’s disease. Jordan J Biol Sci 2017;10(4):257–64.
[41] Ademosun AO, Oboh G. Comparison of the inhibition of monoamine oxidase and butyrylcholinesterase activities by infusions from green tea and some citrus peels. Int J Alzheimers Dis 2014;2014:586407.
[42] Greig NH, Utsuki T, Yu Q, Zhu X, Holloway HW, Perry T, et al. A new therapeutic target in Alzheimer’s disease treatment:attention to butyrylcholinesterase. Curr Med Res Opin 2001;17(3):159–65.
[43] Wang J, Yang Z, Liu L, Zhao Z, Liu Z, Liu X. Protective effect of naringenin against lead-induced oxidative stress in rats. Biol Trace Elem Res 2012;146(3):354–9.
[44] Abdel-Wahhab M, Aly S. Antioxidant property of Nigella sativa(black cumin)and Syzygium aromaticum(clove)in rats during aflatoxicosis. J Appl Toxicol2005;25(3):218–23.
[45] El-Nekeety AA, El-Kady AA, Soliman MS, Hassan NS, Abdel-Wahhab MA.Protective effect of Aquilegia vulgaris(L.)against lead acetate-induced oxidative stress in rats. Food Chem Toxicol 2009;47(9):2209–15.
[46] Ajiboye BO, Akalabu MC, Ojo OA, Afolabi OB, Okesola MA, Olayide I, et al.Inhibitory effect of ethyl acetate fraction of Solanum macrocarpon L. leaves on cholinergic, monoaminergic, and purinergic enzyme activities. J Food Biochem2018;42(6):e12643.
[47] Randrup A, Munkvad I, Pog R. Mania, depression, and brain dopamine. In:Essman W, Valzelli L, editors. Current Developments in Psychopharmacology. New York:Spectrum Publications; 1975. p. 206–48.
[48] Ajiboye BO, Ojo OA, Okesola MA, Oyinloye BE, Kappo AP. Ethyl acetate leaf fraction of Cnidoscolus aconitifolius(Mill.)I. M. Johnst:antioxidant potential,inhibitory activities of key enzymes on carbohydrate metabolism, cholinergic,monoaminergic, purinergic and chemical fingerprinting. Int J Food Prop2018;21(1):1697–715.
[49] Boots AW, Haenen GR, Bast A. Health effects of quercetin:from antioxidant to nutraceutical. Eur J Pharmacol 2008;585:325–37.
[50] Ojo OA, Ajiboye BO, Oyinloye BE, Ojo AB, Olarewaju OI. Protective effect of Irvingia gabonensis stem bark extract on cadmium-induced nephrotoxicity in rats. Interdiscip Toxicol 2014;7(4):208–14.