Galangin ameliorates changes of membrane-bound enzymes in rats with streptozotocin-induced hyperglycemia
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摘要
Objective: To assess the protective effect of galangin on membrane bound enzymes in rats with streptozotocin-induced diabetes. Methods: A single low dose of streptozotocin was injected to adult male albino rats to induce hyperglycemia. Galangin(8 mg/kg) or glibenclamide 600 μg/kg as a standard drug was given orally once daily for 45 days by gavage. Membrane-bound adenosine triphosphatases were determined including total ATPase, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues(kidney, liver, and heart). Results: The levels of total ATPases, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues were significantly altered in diabetic rats as compared to that in normal rats. After 45 days of treatment with galangin or glibenclamide, the levels of these enzymes were similar to that of normal control rats. Conclusions: Oral administration of galangin or glibenclamide can improve activities of these membrane-bound ATPases towards normal levels. Mechanism of galangin needs to be further explored in future.
Objective: To assess the protective effect of galangin on membrane bound enzymes in rats with streptozotocin-induced diabetes. Methods: A single low dose of streptozotocin was injected to adult male albino rats to induce hyperglycemia. Galangin(8 mg/kg) or glibenclamide 600 μg/kg as a standard drug was given orally once daily for 45 days by gavage. Membrane-bound adenosine triphosphatases were determined including total ATPase, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues(kidney, liver, and heart). Results: The levels of total ATPases, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues were significantly altered in diabetic rats as compared to that in normal rats. After 45 days of treatment with galangin or glibenclamide, the levels of these enzymes were similar to that of normal control rats. Conclusions: Oral administration of galangin or glibenclamide can improve activities of these membrane-bound ATPases towards normal levels. Mechanism of galangin needs to be further explored in future.
Objective: To assess the protective effect of galangin on membrane bound enzymes in rats with streptozotocin-induced diabetes. Methods: A single low dose of streptozotocin was injected to adult male albino rats to induce hyperglycemia. Galangin(8 mg/kg) or glibenclamide 600 μg/kg as a standard drug was given orally once daily for 45 days by gavage. Membrane-bound adenosine triphosphatases were determined including total ATPase, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues(kidney, liver, and heart). Results: The levels of total ATPases, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues were significantly altered in diabetic rats as compared to that in normal rats. After 45 days of treatment with galangin or glibenclamide, the levels of these enzymes were similar to that of normal control rats. Conclusions: Oral administration of galangin or glibenclamide can improve activities of these membrane-bound ATPases towards normal levels. Mechanism of galangin needs to be further explored in future.
引文
[1]World Health Organization.The top 10 causes of death.[Online]Available from:https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death[Accessed on 24 May 2018].
[2]Bajaj HS,Zinman B.Glucose lowering strategies for cardiac benefits:Pathophysiological mechanisms.Physiology(Bethesda)2018;33(3):197-210.
[3]WHO.Global report on diabetes.[Online]Available from:https://www.who.int/diabetes/global-report/en/[Accessed on 7 April 2016].
[4]Reddy PM,Philip GH.Changes in the levels of respiration and ions in the tissues of freshwater fish,under fenvalerate stress.Chemosphere 1992;25(6):843-852.
[5]Chang KC,Chung SY,Chong WS,Suh JS,Kim SH,Noh HK,et al.Possible superoxide radical-induced alteration of vascular reactivity in aortas from streptozotocin-treated rats.J Pharmacol Exp Ther 1993;266(2):992-1000.
[6]Jain SK.Hyperglycemia can cause membrane lipid peroxidation and osmotic fragility in human red blood cells.J Biol Chem 1989;264(35):21340-21345.
[7]RauchováH,LedvinkováJ,Kalous M,Drahota Z.The effect of lipid peroxidation on the activity of various membrane-bound ATPases in rat kidney.Int J Biochem Cell Biol 1995;27(3):251-255.
[8]Yessoufou A,Gbenou J,Grissa O,Hichami A,Simonin AM,Tabka Z,et al.Anti-hyperglycemic effects of three medicinal plants in diabetic pregnancy:Modulation of T cell proliferation.BMC Complement Altern Med 2013;13:77.
[9]Tiwari BK,Kumar D,Abidi AB,Rizvi SI.Efficacy of composite extract from leaves and fruits of medicinal plants used in traditional diabetic therapy against oxidative stress in alloxan-induced diabetic rats.ISRNPharmacol 2014;2014:608590.
[10]Michael HN,Salib JY,Eskander EF.Bioactivity of diosmetin glycosides isolated from the epicarp of date fruits,Phoenix dactylifera,on the biochemical profile of alloxan diabetic male rats.Phytother Res 2013;27(5):699-704.
[11]Duarte J,Pérez-Palencia R,Vargas F,Ocete MA,Pérez-Vizcaino F,Zarzuelo A,et al.Antihypertensive effects of the flavonoid quercetin in spontaneously hypertensive rats.Br J Pharmacol 2001;133(1):117-124.290
[12]Su CH,Kuo CL,Lu KW,Yu FS,Ma YS,Yang JL,et al.Fisetininduced apoptosis of human oral cancer SCC-4 cells through reactive oxygen species production,endoplasmic reticulum stress,caspase-,and mitochondria-dependent signaling pathways.Environ Toxicol 2017;32(6):1725-1741.
[13]Akachi T,Shiina Y,Ohishi Y,Kawaguchi T,Kawagishi H,Morita T,et al.Hepatoprotective effects of flavonoids from shekwasha(Citrus depressa)against D-galactosamine-induced liver injury in rats.J Nutr Sci Vitaminol2010;56(1):60-67.
[14]Aloud AA,Veeramani C,Govindasamy C,Alsaif MA,El Newehy AS,Al-Numair KS.Galangin,a dietary flavonoid,improves antioxidant status and reduces hyperglycemia-mediated oxidative stress in streptozotocininduced diabetic rats.Redox Rep 2017;22(6):290-300.
[15]Jung YC,Kim ME,Yoon JH,Park PR,Youn HY,Lee HW,et al.Antiinflammatory effects of galangin on lipopolysaccharide-activated macrophages via ERK and NF-κB pathway regulation.Immunopharmacol Immunotoxicol 2014;36(6):426-432.
[16]Sivakumar AS,Anuradha CV.Effect of galangin supplementation on oxidative damage and inflammatory changes in fructose-fed rat liver.Chem Biol Interact 2011;193(2):141-148.
[17]Lei YF,Chen JL,Zhang WT,Fu W,Wu GH,Wei H,et al.In vivo investigation on the potential of galangin,kaempferol and myricetin for protection of D-galactose-induced cognitive impairment.Food Chem2012;135(4):2702-2707.
[18]Murakami S,Muramatsu M,Otomo S.Inhibition of gastric H+,K(+)-ATPase by quercetin.J Enzym Inhib 1992;5(4):293-298.
[19]Szkudelski T.The mechanism of alloxan and streptozotocin action in Bcells of the rat pancreas.Physiol Res 2001;50(6):537-546.
[20]Trinder P.Determination of glucose in blood using glucose oxidase with an alternative oxygen acceptor.Ann Clin Biochem 1969;6(1):24-27.
[21]Lowry OH,Rosebrough NJ,Farr AL,Randall RJ.Protein measurement with the Folin phenol reagent.J Biol Chem 1951;193(1):265-275.
[22]Evans DJ Jr.Membrane adenosine triphosphatase of Escherichia coli:Activation by calcium ion and inhibition by monovalent cations.JBacteriol 1969;100(2):914-922.
[23]Bonting SL.Sodium-potassium activated adenosine-triphosphatase and cation transport.In:Bittar C(ed).Membrane and iron transport.London:Wiley Interscience;1970,p.25-28.
[24]Hjertén S,Pan H.Purification and characterization of two forms of a low-affinity Ca2+-ATPase from erythrocyte membranes.Biochim Biophys Acta 1983;728(2):281-288.
[25]Ohnishi T,Suzuki T,Suzuki Y,Ozawa K.A comparative study of plasma membrane Mg2+-ATPase activities in normal,regenerating and malignant cells.Biochim Biophys Acta 1982;684(1):67-74.
[26]Aronson D,Rayfield EJ.How hyperglycemia promotes atherosclerosis:Molecular mechanisms.Cardiovasc Diabetol 2002;1:1.
[27]Yan LJ.Pathogenesis of chronic hyperglycemia:From reductive stress to oxidative stress.J Diabetes Res 2014;2014:137919.
[28]Suhail M.Na,K-ATPase:Ubiquitous multifunctional transmembrane protein and its relevance to various pathophysiological conditions.J Clin Med Res 2010;2(1):1-17.
[29]Haynes DH.Mechanism of Ca2+transport by Ca2+-Mg2+-ATPase pump:Analysis of major states and pathways.Am J Physiol 1983;244(1):G3-12.
[30]Namazi G,Jamshidi Rad S,Attar AM,Sarrafzadegan N,Sadeghi M,Naderi G,et al.Increased membrane lipid peroxidation and decreased Na+/K+-ATPase activity in erythrocytes of patients with stable coronary artery disease.Coron Artery Dis 2015;26(3):239-244.
[31]Vér A,SzántóI,Bányász T,Csermely P,Végh E,Somogyi J.Changes in the expression of Na+/K+-ATPase isoenzymes in the left ventricle of diabetic rat hearts:Effect of insulin treatment.Diabetologia 1997;40(11):1255-1262.
[32]Sweeney G,Klip A.Regulation of the Na+/K+-ATPase by insulin:Why and how?Mol Cell Biochem 1998;182(1-2):121-133.
[33]Al-Numair KS,Veeramani C,Alsaif MA,Chandramohan G.Influence of kaempferol,a flavonoid compound,on membrane-bound ATPases in streptozotocin-induced diabetic rats.Pharm Biol 2015;53(9):1372-1378.
[34]Davis SM,Maddux AB,Alonso GT,Okada CR,Mourani PM,Maahs DM.Profound hypokalemia associated with severe diabetic ketoacidosis.Pediatr Diabetes 2016;17(1):61-65.
[35]Goldberg IJ.Diabetic dyslipidemia:Causes and consequences.J Clin Endocrinol Metab 2001;86(3):965-971.
[36]Gupta S,Phipps K,Ruderman NB.Differential stimulation of Na+pump activity by insulin and nitric oxide in rabbit aorta.Am J Physiol 1996;270(4 Pt 2):H1287-H1293.
[37]van Heeswijk MP,Geertsen JA,van Os CH.Kinetic properties of the ATP-dependent Ca2+pump and the Na+/Ca2+exchange system in basolateral membranes from rat kidney cortex.J Membr Biol 1984;79(1):19-31.
[38]Hope-Gill HF,Nanda V.Stimulation of calcium ATPase by insulin,glucagon,cyclic AMP and cyclic GMP in Triton X-100 extracts of purified rat liver plasma membrane.Horm Metab Res 1979;11(12):698-700.
[39]Levy J,Rempinski D,Kuo TH.Hormone-specific defect in insulin regulation of(Ca2++Mg2+)-adenosine triphosphatase activity in kidney membranes from streptozocin non-insulin-dependent diabetic rats.Metab Clin Exp 1994;43(5):604-613.
[40]Jain SK,Lim G.Lipoic acid decreases lipid peroxidation and protein glycosylation and increases(Na(+)+K(+))-and Ca(++)-ATPase activities in high glucose-treated human erythrocytes.Free Radic Biol Med 2000;29(11):1122-1128.
[41]Otake Y,Walle T.Oxidation of the flavonoids galangin and kaempferide by human liver microsomes and CYP1A1,CYP1A2,and CYP2C9.Drug Metab Dispos 2002;30(2):103-105.
[2]Bajaj HS,Zinman B.Glucose lowering strategies for cardiac benefits:Pathophysiological mechanisms.Physiology(Bethesda)2018;33(3):197-210.
[3]WHO.Global report on diabetes.[Online]Available from:https://www.who.int/diabetes/global-report/en/[Accessed on 7 April 2016].
[4]Reddy PM,Philip GH.Changes in the levels of respiration and ions in the tissues of freshwater fish,under fenvalerate stress.Chemosphere 1992;25(6):843-852.
[5]Chang KC,Chung SY,Chong WS,Suh JS,Kim SH,Noh HK,et al.Possible superoxide radical-induced alteration of vascular reactivity in aortas from streptozotocin-treated rats.J Pharmacol Exp Ther 1993;266(2):992-1000.
[6]Jain SK.Hyperglycemia can cause membrane lipid peroxidation and osmotic fragility in human red blood cells.J Biol Chem 1989;264(35):21340-21345.
[7]RauchováH,LedvinkováJ,Kalous M,Drahota Z.The effect of lipid peroxidation on the activity of various membrane-bound ATPases in rat kidney.Int J Biochem Cell Biol 1995;27(3):251-255.
[8]Yessoufou A,Gbenou J,Grissa O,Hichami A,Simonin AM,Tabka Z,et al.Anti-hyperglycemic effects of three medicinal plants in diabetic pregnancy:Modulation of T cell proliferation.BMC Complement Altern Med 2013;13:77.
[9]Tiwari BK,Kumar D,Abidi AB,Rizvi SI.Efficacy of composite extract from leaves and fruits of medicinal plants used in traditional diabetic therapy against oxidative stress in alloxan-induced diabetic rats.ISRNPharmacol 2014;2014:608590.
[10]Michael HN,Salib JY,Eskander EF.Bioactivity of diosmetin glycosides isolated from the epicarp of date fruits,Phoenix dactylifera,on the biochemical profile of alloxan diabetic male rats.Phytother Res 2013;27(5):699-704.
[11]Duarte J,Pérez-Palencia R,Vargas F,Ocete MA,Pérez-Vizcaino F,Zarzuelo A,et al.Antihypertensive effects of the flavonoid quercetin in spontaneously hypertensive rats.Br J Pharmacol 2001;133(1):117-124.290
[12]Su CH,Kuo CL,Lu KW,Yu FS,Ma YS,Yang JL,et al.Fisetininduced apoptosis of human oral cancer SCC-4 cells through reactive oxygen species production,endoplasmic reticulum stress,caspase-,and mitochondria-dependent signaling pathways.Environ Toxicol 2017;32(6):1725-1741.
[13]Akachi T,Shiina Y,Ohishi Y,Kawaguchi T,Kawagishi H,Morita T,et al.Hepatoprotective effects of flavonoids from shekwasha(Citrus depressa)against D-galactosamine-induced liver injury in rats.J Nutr Sci Vitaminol2010;56(1):60-67.
[14]Aloud AA,Veeramani C,Govindasamy C,Alsaif MA,El Newehy AS,Al-Numair KS.Galangin,a dietary flavonoid,improves antioxidant status and reduces hyperglycemia-mediated oxidative stress in streptozotocininduced diabetic rats.Redox Rep 2017;22(6):290-300.
[15]Jung YC,Kim ME,Yoon JH,Park PR,Youn HY,Lee HW,et al.Antiinflammatory effects of galangin on lipopolysaccharide-activated macrophages via ERK and NF-κB pathway regulation.Immunopharmacol Immunotoxicol 2014;36(6):426-432.
[16]Sivakumar AS,Anuradha CV.Effect of galangin supplementation on oxidative damage and inflammatory changes in fructose-fed rat liver.Chem Biol Interact 2011;193(2):141-148.
[17]Lei YF,Chen JL,Zhang WT,Fu W,Wu GH,Wei H,et al.In vivo investigation on the potential of galangin,kaempferol and myricetin for protection of D-galactose-induced cognitive impairment.Food Chem2012;135(4):2702-2707.
[18]Murakami S,Muramatsu M,Otomo S.Inhibition of gastric H+,K(+)-ATPase by quercetin.J Enzym Inhib 1992;5(4):293-298.
[19]Szkudelski T.The mechanism of alloxan and streptozotocin action in Bcells of the rat pancreas.Physiol Res 2001;50(6):537-546.
[20]Trinder P.Determination of glucose in blood using glucose oxidase with an alternative oxygen acceptor.Ann Clin Biochem 1969;6(1):24-27.
[21]Lowry OH,Rosebrough NJ,Farr AL,Randall RJ.Protein measurement with the Folin phenol reagent.J Biol Chem 1951;193(1):265-275.
[22]Evans DJ Jr.Membrane adenosine triphosphatase of Escherichia coli:Activation by calcium ion and inhibition by monovalent cations.JBacteriol 1969;100(2):914-922.
[23]Bonting SL.Sodium-potassium activated adenosine-triphosphatase and cation transport.In:Bittar C(ed).Membrane and iron transport.London:Wiley Interscience;1970,p.25-28.
[24]Hjertén S,Pan H.Purification and characterization of two forms of a low-affinity Ca2+-ATPase from erythrocyte membranes.Biochim Biophys Acta 1983;728(2):281-288.
[25]Ohnishi T,Suzuki T,Suzuki Y,Ozawa K.A comparative study of plasma membrane Mg2+-ATPase activities in normal,regenerating and malignant cells.Biochim Biophys Acta 1982;684(1):67-74.
[26]Aronson D,Rayfield EJ.How hyperglycemia promotes atherosclerosis:Molecular mechanisms.Cardiovasc Diabetol 2002;1:1.
[27]Yan LJ.Pathogenesis of chronic hyperglycemia:From reductive stress to oxidative stress.J Diabetes Res 2014;2014:137919.
[28]Suhail M.Na,K-ATPase:Ubiquitous multifunctional transmembrane protein and its relevance to various pathophysiological conditions.J Clin Med Res 2010;2(1):1-17.
[29]Haynes DH.Mechanism of Ca2+transport by Ca2+-Mg2+-ATPase pump:Analysis of major states and pathways.Am J Physiol 1983;244(1):G3-12.
[30]Namazi G,Jamshidi Rad S,Attar AM,Sarrafzadegan N,Sadeghi M,Naderi G,et al.Increased membrane lipid peroxidation and decreased Na+/K+-ATPase activity in erythrocytes of patients with stable coronary artery disease.Coron Artery Dis 2015;26(3):239-244.
[31]Vér A,SzántóI,Bányász T,Csermely P,Végh E,Somogyi J.Changes in the expression of Na+/K+-ATPase isoenzymes in the left ventricle of diabetic rat hearts:Effect of insulin treatment.Diabetologia 1997;40(11):1255-1262.
[32]Sweeney G,Klip A.Regulation of the Na+/K+-ATPase by insulin:Why and how?Mol Cell Biochem 1998;182(1-2):121-133.
[33]Al-Numair KS,Veeramani C,Alsaif MA,Chandramohan G.Influence of kaempferol,a flavonoid compound,on membrane-bound ATPases in streptozotocin-induced diabetic rats.Pharm Biol 2015;53(9):1372-1378.
[34]Davis SM,Maddux AB,Alonso GT,Okada CR,Mourani PM,Maahs DM.Profound hypokalemia associated with severe diabetic ketoacidosis.Pediatr Diabetes 2016;17(1):61-65.
[35]Goldberg IJ.Diabetic dyslipidemia:Causes and consequences.J Clin Endocrinol Metab 2001;86(3):965-971.
[36]Gupta S,Phipps K,Ruderman NB.Differential stimulation of Na+pump activity by insulin and nitric oxide in rabbit aorta.Am J Physiol 1996;270(4 Pt 2):H1287-H1293.
[37]van Heeswijk MP,Geertsen JA,van Os CH.Kinetic properties of the ATP-dependent Ca2+pump and the Na+/Ca2+exchange system in basolateral membranes from rat kidney cortex.J Membr Biol 1984;79(1):19-31.
[38]Hope-Gill HF,Nanda V.Stimulation of calcium ATPase by insulin,glucagon,cyclic AMP and cyclic GMP in Triton X-100 extracts of purified rat liver plasma membrane.Horm Metab Res 1979;11(12):698-700.
[39]Levy J,Rempinski D,Kuo TH.Hormone-specific defect in insulin regulation of(Ca2++Mg2+)-adenosine triphosphatase activity in kidney membranes from streptozocin non-insulin-dependent diabetic rats.Metab Clin Exp 1994;43(5):604-613.
[40]Jain SK,Lim G.Lipoic acid decreases lipid peroxidation and protein glycosylation and increases(Na(+)+K(+))-and Ca(++)-ATPase activities in high glucose-treated human erythrocytes.Free Radic Biol Med 2000;29(11):1122-1128.
[41]Otake Y,Walle T.Oxidation of the flavonoids galangin and kaempferide by human liver microsomes and CYP1A1,CYP1A2,and CYP2C9.Drug Metab Dispos 2002;30(2):103-105.