Cinnamaldehyde Attenuates Cataractogenesis via Restoration of Hypertension and Oxidative Stress in Fructose-Fed Hypertensive rats
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Objectives: Several studies have revealed that systemic hypertension is strongly associated with cataractogenesis. However, the pathophysiology and treatment is often unclear. In this study, we evaluated the anti-cataractogenic effect of cinnamaldehyde (CA), a natural organic compound, in rats with fructose-induced hypertension. Methods: The rats were divided into six groups. For six weeks, the normal group received a suspension of 0.5% carboxy methyl cellulose (10 mL/kg/day, p.o.) while five other groups received a 10% (w/v) fructose solution in their drinking water to induce hypertension. By the end of the third week hypertension had been induced in all the animals receiving fructose. From the beginning of the fourth week to the end of the sixth week, one of those five groups (control) continued to receive only 10% (w/v) fructose solution, one group (standard) received ramipril (1 mg/kg/day, p.o.) plus 10% (w/v) fructose solution, and three groups (experimental) received CA at doses of 20, 30, and 40 mg/kg/day p.o., plus 10% (w/v) fructose solution. Blood pressure was measured weekly using a non-invasive blood pressure apparatus. After six weeks, the animals were sacrificed, and the anti-cataractogenic effects on the eye lenses were evaluated. Results: Administration of fructose elevated both the systolic and the diastolic blood pressures, which were significantly reduced by CA at all dose levels. In the control group, a significant increase in the malonaldehyde (MDA) level and decreases in the total protein, Ca2+adenosine triphosphate (ATP)ase activity, glutathione peroxidase, catalase, superoxide dismutase and glutathione levels, as compared to the normal group, were observed. Administration of CA at all doses significantly restored the enzymatic, non-enzymatic, antioxidants, total protein, and Ca2+ATPase levels, but decreased the MDA level, as compared to the control group. Conclusion: The present study revealed that CA modulated the antioxidant parameters of the serum and lens homogenates in hypertension-induced cataractogenic animals.
Abstract
Objectives: Several studies have revealed that systemic hypertension is strongly associated with cataractogenesis. However, the pathophysiology and treatment is often unclear. In this study, we evaluated the anti-cataractogenic effect of cinnamaldehyde (CA), a natural organic compound, in rats with fructose-induced hypertension. Methods: The rats were divided into six groups. For six weeks, the normal group received a suspension of 0.5% carboxy methyl cellulose (10 mL/kg/day, p.o.) while five other groups received a 10% (w/v) fructose solution in their drinking water to induce hypertension. By the end of the third week hypertension had been induced in all the animals receiving fructose. From the beginning of the fourth week to the end of the sixth week, one of those five groups (control) continued to receive only 10% (w/v) fructose solution, one group (standard) received ramipril (1 mg/kg/day, p.o.) plus 10% (w/v) fructose solution, and three groups (experimental) received CA at doses of 20, 30, and 40 mg/kg/day p.o., plus 10% (w/v) fructose solution. Blood pressure was measured weekly using a non-invasive blood pressure apparatus. After six weeks, the animals were sacrificed, and the anti-cataractogenic effects on the eye lenses were evaluated. Results: Administration of fructose elevated both the systolic and the diastolic blood pressures, which were significantly reduced by CA at all dose levels. In the control group, a significant increase in the malonaldehyde (MDA) level and decreases in the total protein, Ca2+adenosine triphosphate (ATP)ase activity, glutathione peroxidase, catalase, superoxide dismutase and glutathione levels, as compared to the normal group, were observed. Administration of CA at all doses significantly restored the enzymatic, non-enzymatic, antioxidants, total protein, and Ca2+ATPase levels, but decreased the MDA level, as compared to the control group. Conclusion: The present study revealed that CA modulated the antioxidant parameters of the serum and lens homogenates in hypertension-induced cataractogenic animals.
참고문헌 (51)
- Lira RP, "Incidence of preoperative high blood pressure in cataract surgery among hypertensive and normotensive patients", Indian J Opthalmol, 58(6), pp.493~495 (2010)
- Kearney PM, "Global burden of hypertension: analysis of worldwide data", Lancet, 365(9455), pp.217~223 (2005)
- Lin L, "Angiotensin-I-converting enzyme (ACE)-inhibitory and antihypertensive properties of squid skin gelatin hydrolysates", Food Chem, 131(1), pp.225~230 (2012)
- Mukesh BN, "Development of cataract and associated risk factors", Arch Ophthalmol, 124(1), pp.79~85 (2006)
- Tyler Hyung Taek Rim, "Cataract subtype risk factors identified from the Korea National Health and Nutrition Examination survey 2008–2010", BMC Ophthalmology, 14(1) (2014), Springer Nature[DOI]
- Tsai SY, "Epidemiologic study of age-related cataracts among an elderly Chinese population in Shih-Pai, Taiwan", Ophthalmology, 110(6), pp.1089~1095 (2003)
- Xiaoning Yu, "Hypertension and Risk of Cataract: A Meta-Analysis", PLoS ONE, 9(12), pp.e114012~ (2014), Public Library of Science (PLoS)[DOI]
- Wong TY, "The eye in hypertension", Lancet, 369(9559), pp.425~435 (2007)
- Bautista LE, "Independent association between inflammatory markers (C-reactive protein, interleukin-6, and TNF-alpha) and essential hypertension", J Hum Hypertension, 19(2), pp.149~154 (2005)
- Schaumberg DA, "High levels of plasma C-reactive protein and future risk of age-related cataract", Ann Epidemiol, 9(3), pp.166~171 (1999)
- Lee SM, "Possible mechanism of exacerbating cataract formation in cataractous human lens capsules induced by systemic hypertension or glaucoma", Ophthalmic Res, 29(2), pp.83~90 (1997)
- Klein AV, "The mechanisms underlying fructose-induced hypertension : a review", J Hypertens, 33(5), pp.912~920 (2015)
- Balasaraswathi K, "Changes in redox ratio and protein glycation in precataractous lens from fructose-fed rats : effects of exogenous L-carnitine", Clin Exp Pharmacol Physiol, 35(2), pp.168~173 (2008)
- Mang B, "Effects of a cinnamon extract on plasma glucose, HbA1c and serum lipids in diabetes mellitus type 2", Eur J Clin Invest, 36(5), pp.340~344 (2006)
- Mahfouz MH, "Therapeutic effect of L-carnitine on sialic acid, soluble Fas(sFas)and other biochemical variables in hyperinsulinemic rats", Life Sci J, 6(2), pp.76~82 (2009)
- El-Bassossy HM, "Cinnamaldehyde protects from the hypertension associated with diabetes", Food Chem Toxicol, 49(11), pp.3007~3012 (2011)
- Chang ST, "Antibacterial activity of leaf essential oils and their constituents from Cinnamomum osmophloeum", J Ethnopharmacol, 77(1), pp.123~127 (2001)
- Chao LK, "Cinnamaldehyde inhibits pro-inflammatory cytokines secretion frommonocytes", macrophages through suppression of intracellular signaling, 2008, pp.46(1), 220~231
- Youn HS, "Cinnamaldehyde suppresses toll-like receptor 4 activation mediated through the inhibition of receptor oligomerization", Biochem Pharmacol, 75(2), pp.494~502 (2008)
- Zhang W, "Anti-diabetic effects of cinnamaldehyde and berberine and their impacts on retinol-binding protein 4expression in rats with type 2 diabetes mellitus", Chin Med J(Engl), 121(21), pp.2124~2128 (2008)
- Lee HS, "Inhibitory activity of Cinnamomum cassia bark-derived component against rat lens aldose reductase", J Pharm Pharm Sci, 5(3), pp.226~230 (2002)
- Dai S, "Fructose-induced hypertension in rats is concentration and duration dependent", J Pharmacol Toxicol Methods, 33(2), pp.101~107 (1995)
- Son HY, "Taurine prevents oxidative damage of high glucose – induced cataractogenesis in isolated rat lenses", J Nutr Sci Vitaminol, 53(4), pp.324~330 (2007)
- Tappel AL, "Glutathione peroxidase and hydroperoxides", Methods Enzymol, 52(53), pp.506~513 (1978)
- Aebi H, "Catalase in vitro", Methods Enzymol, 105, pp.121~126 (1984)
- Kakkar P, "A modified spectrophotometric assay of superoxide dismutase", Indian J Biochem Biophys, 21(2), pp.130~132 (1984)
- Ellman GL, "Tissue sulfhydryl groups", Arch Biochem Biophys, 82(1), pp.70~77 (1959)
- Ohkawa H, "Assay of lipid peroxide in animal tissue by thiobarbituric acid reaction", Anal Biochem, 95(2), pp.351~358 (1979)
- Lowry OH, "Protein measurement with Folin phenol reagent", J Biol Chem, 193(1), pp.265~275 (1951)
- Rorive G, "Ca2+-Activated ATPase from renal tubular cells", Methods Enzymol, 32(28), pp.303~306 (1974)
- de Champlain J, "Oxidative stress in hypertension", Clin Exp Hypertens, 26(7-8), pp.593~601 (2004)
- Redon J, "Antioxidant activities and oxidative stress byproducts in human hypertension", Hypertension, 41(5), pp.1096~1101 (2003)
- Dimo T, "Leaf methanol extract of Bidens pilosa prevents and attenuates the hypertension induced by high-fructose diet in Wistar rats", J Ethnopharmacol, 83(3), pp.183~191 (2002)
- Khitan Z, "Fructose: a key factor in the development of metabolic syndrome and hypertension", J Nutr Metab, 2013 (2013)[DOI]
- Brownlee M, "The pathobiology of diabetic complications: a unifying mechanism", Diabetes, 54(6), pp.1615~1625 (2005)
- Rebolledo OR, "Abdominal adipose tissue: early metabolic dysfunction associated to insulin resistance and oxidative stress induced by an unbalanced diet", Horm Metab Res, 40(11), pp.794~800 (2008)
- Gersch MS, "Fructose, but not dextrose, accelerates the progression of chronic kidney disease", Am J Physiol Renal physiol, 293(4), pp.1256~1261 (2007)
- Rajasekar P, "Effect of L-carnitine on skeletal muscle lipids and oxidative stress in rats fed high-fructose diet", Exp Diabetes Res, 2007, pp.72741~ (2007)
- Guglielmotto M, "AGEs", RAGE complex upregulates BACE1 via NF-kappa B pathway activation, 2012, pp.33(1), 13~27
- Lyle BJ, "Antioxidant intake and risk of incident age-related nuclear cataracts in the beaver dam eye study", Am J Epidemiol, 149(9), pp.801~809 (1999)
- Takagi Y, "Significance of fructose-induced protein oxidation and formation of advanced glycation end product", J Diabetes Complications, 9(2), pp.87~91 (1995)
- Paglia DE, "Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase", J Lab Clin Med, 70(1), pp.158~169 (1967)
- Shearer TR, "Amelioration of cataracts and proteolysis in cultured lenses by cysteine protease inhibitor E64", Invest Ophthalmol Vis Sci, 32(3), pp.533~540 (1991)
- Awasthi S, "Curcumin protects against 4-hydroxy- 2-trans-nonenal-induced cataract formation in rat lenses", AM J Clin Nutr, 64(5), pp.761~766 (1996)
- Grattagliano I, "Oxidative retinal products and ocular damages in diabetic patients", Free Radic Biol Med, 25(3), pp.369~372 (1998)
- Gupta PD, "Causative and preventive action of calcium in cataracto-genesis", Acta Pharmacol Sin, 25(10), pp.1250~1256 (2004)
- Liu L, "Regulation of sarco", endoplasmic Ca2+-ATPase expression by calcium in human lens cells, 2002, pp.75(5), 583~590
- Bodakhe SH, "Anticataract activity of rhamnocitrin isolated from Bauhinia variegata stem bark", Orient Pharm Exp Med, 12(3), pp.227~232 (2012)
- Jung HA, "Extraction and identification of three major aldose reductase inhibitors from Artemisia montana", Food Chem Toxicol, 49(2), pp.376~384 (2011)
- Lee AY, "Demonstration that polyol accumulation is responsible for diabetic cataract by the use of transgenic mice expressing the aldose reductase gene in the lens", Proc Natl Acad Sci USA, 92(7), pp.2780~2784 (1995)
- Lee HS, "Inhibitory activity of Cinnamomum cassia bark-derived component against rat lens aldose reductase", J Pharm Pharm Sci, 5(3), pp.226~230 (2002)