Skip to main content
Top
Published in: Cardiovascular Toxicology 1/2019

01-02-2019

Beneficial Effect of Silymarin in Pressure Overload Induced Experimental Cardiac Hypertrophy

Authors: Basant Sharma, Udit Chaube, Bhoomika M. Patel

Published in: Cardiovascular Toxicology | Issue 1/2019

Login to get access

Abstract

The present investigation was undertaken to study the effect of silymarin on cardiac hypertrophy induced by partial abdominal aortic constriction (PAAC) in Wistar rats. Silymarin was administered for 9 weeks at the end of which we evaluated hypertrophic, hemodynamic, non-specific cardiac markers, oxidative stress parameters, and determined mitochondrial DNA concentration. Hypertrophic control animals exhibited cardiac hypertrophy, altered hemodynamics, oxidative stress, and decreased mitochondrial DNA (mtDNA) concentration. Treatment with silymarin prevented cardiac hypertrophy, improved hemodynamic functions, prevented oxidative stress and increased mitochondrial DNA concentration. Docking studies revealed that silymarin produces maximum docking score with mitogen-activated protein kinases (MAPK) p38 as compared to other relevant proteins docked. Moreover, PAAC-control rats exhibited significantly increased expression of MAPK p38β mRNA levels which were significantly decreased by the treatment of silymarin. Our data suggest that silymarin produces beneficial effects on cardiac hypertrophy which are likely to be mediated through inhibition of MAPK p38β.
Literature
1.
go back to reference Anan, R., Nakagawa, M., Miyata, M., Higuchi, I., Nakao, S., Suehara, M., et al. (1995). Cardiac involvement in mitochondrial diseases. A study on 17 patients with documented mitochondrial DNA defects. Circulation, 91(4), 955–961.CrossRef Anan, R., Nakagawa, M., Miyata, M., Higuchi, I., Nakao, S., Suehara, M., et al. (1995). Cardiac involvement in mitochondrial diseases. A study on 17 patients with documented mitochondrial DNA defects. Circulation, 91(4), 955–961.CrossRef
2.
go back to reference Andrews, C., Ho, P., Dillmann, W., Glembotski, C., & McDonoughc, P. (2003). The MKK6–p38 MAPK pathway prolongs the cardiac contractile calcium transient, downregulates SERCA2, and activates NF-AT. Cardiovascular Research, 59, 46–56.CrossRef Andrews, C., Ho, P., Dillmann, W., Glembotski, C., & McDonoughc, P. (2003). The MKK6–p38 MAPK pathway prolongs the cardiac contractile calcium transient, downregulates SERCA2, and activates NF-AT. Cardiovascular Research, 59, 46–56.CrossRef
3.
go back to reference Anton, R., Bauer, S. M., Keck, P., & Laufer, P. (2014). A p38 Substrate-Specific MK2-EGFP translocation assay for identification and validation of new p38 inhibitors in living cells: A comprising alternative for acquisition of cellular p38 inhibition. PLoS ONE, 9, e95641.CrossRef Anton, R., Bauer, S. M., Keck, P., & Laufer, P. (2014). A p38 Substrate-Specific MK2-EGFP translocation assay for identification and validation of new p38 inhibitors in living cells: A comprising alternative for acquisition of cellular p38 inhibition. PLoS ONE, 9, e95641.CrossRef
4.
go back to reference Barja, G., & Herrero, A. (2000). Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heat and brain of mammals. The FASEB Journal, 14, 312–318.CrossRef Barja, G., & Herrero, A. (2000). Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heat and brain of mammals. The FASEB Journal, 14, 312–318.CrossRef
5.
go back to reference Bernardo, B. C., Weeks, K. L., Pretorius, L., & McMullen Jr. (2010). Molecular distinction between physiological and pathological cardiac hypertrophy: Experimental findings and therapeutic strategies. Pharmacology & Therapeutics, 128, 191–227.CrossRef Bernardo, B. C., Weeks, K. L., Pretorius, L., & McMullen Jr. (2010). Molecular distinction between physiological and pathological cardiac hypertrophy: Experimental findings and therapeutic strategies. Pharmacology & Therapeutics, 128, 191–227.CrossRef
6.
go back to reference Borah, A., Paul, R., Choudhury, S., Choudhury, A., Bhuyan, B., Talukdar, D., A., et al (2013). Neuroprotective potential of silymarin against CNS disorders: Insight into the pathways and molecular mechanisms of action. CNS Neuroscience Therapeutics, 19, 847–853.CrossRef Borah, A., Paul, R., Choudhury, S., Choudhury, A., Bhuyan, B., Talukdar, D., A., et al (2013). Neuroprotective potential of silymarin against CNS disorders: Insight into the pathways and molecular mechanisms of action. CNS Neuroscience Therapeutics, 19, 847–853.CrossRef
7.
go back to reference Buckley, D. I., Fu, R., Freeman, M., Rogers, K., & Helfand, M. (2009). C-reactive protein as a risk factor for coronary heart disease: A systematic review and meta-analyses for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 151, 483–495.CrossRef Buckley, D. I., Fu, R., Freeman, M., Rogers, K., & Helfand, M. (2009). C-reactive protein as a risk factor for coronary heart disease: A systematic review and meta-analyses for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 151, 483–495.CrossRef
8.
go back to reference Bugger, H., & Abel, E. D. (2010). Mitochondria in the diabetic heart. Cardiovascular Research, 88, 229–240.CrossRef Bugger, H., & Abel, E. D. (2010). Mitochondria in the diabetic heart. Cardiovascular Research, 88, 229–240.CrossRef
9.
go back to reference Chen, P. N., Hsieh, Y. S., Chiou, H. L., & Chu, S. C. (2005). Silibinin inhibits cell invasion through inactivation of both PI3K-Akt and MAPK signaling pathways. Chemico-Biological Interactions, 156(2–3), 141–150.CrossRef Chen, P. N., Hsieh, Y. S., Chiou, H. L., & Chu, S. C. (2005). Silibinin inhibits cell invasion through inactivation of both PI3K-Akt and MAPK signaling pathways. Chemico-Biological Interactions, 156(2–3), 141–150.CrossRef
10.
go back to reference Dai, D. F., Johnson, S. C., Villarin, J. J., Chin, M. T., Nieves-Cintron, M., Chen, T., et al. (2011). Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure. Circulation Research, 108, 837–846.CrossRef Dai, D. F., Johnson, S. C., Villarin, J. J., Chin, M. T., Nieves-Cintron, M., Chen, T., et al. (2011). Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure. Circulation Research, 108, 837–846.CrossRef
11.
go back to reference Dhalla, N. S., Temsah, R. M., & Netticadan, T. (2000). Role of oxidative stress in cardiovascular diseases. Journal of Hypertension, 18, 655–673.CrossRef Dhalla, N. S., Temsah, R. M., & Netticadan, T. (2000). Role of oxidative stress in cardiovascular diseases. Journal of Hypertension, 18, 655–673.CrossRef
12.
go back to reference Dickhout, J. G., Carlisle, R. E., & Austin, R. C. (2011). Interrelationship between cardiac hypertrophy, heart failure, and chronic kidney disease: Endoplasmic reticulum stress as a mediator of pathogenesis. Circulation Research, 108(5), 629–642.CrossRef Dickhout, J. G., Carlisle, R. E., & Austin, R. C. (2011). Interrelationship between cardiac hypertrophy, heart failure, and chronic kidney disease: Endoplasmic reticulum stress as a mediator of pathogenesis. Circulation Research, 108(5), 629–642.CrossRef
13.
go back to reference Elkamhawy, A., Lee, J., Park, B. G., Park, I., Pae, A. N., & Roh, E. J. (2014). Novel quinazoline-urea analogues as modulators for Aβ-induced mitochondrial dysfunction: Design, synthesis, and molecular docking study. European Journal of Medicinal Chemistry, 84, 466–475.CrossRef Elkamhawy, A., Lee, J., Park, B. G., Park, I., Pae, A. N., & Roh, E. J. (2014). Novel quinazoline-urea analogues as modulators for Aβ-induced mitochondrial dysfunction: Design, synthesis, and molecular docking study. European Journal of Medicinal Chemistry, 84, 466–475.CrossRef
14.
go back to reference Frey, N., & Olson, E. N. (2003). Cardiac hypertrophy: The good, the bad, and the ugly. Annual Review of Physiology, 65, 45–79.CrossRef Frey, N., & Olson, E. N. (2003). Cardiac hypertrophy: The good, the bad, and the ugly. Annual Review of Physiology, 65, 45–79.CrossRef
15.
go back to reference Gabrielová, E., Zholobenko, A. V., Bartošíková, L., Nečas, J., & Modriansky, M. (2015). Silymarin constituent 2,3-dehydrosilybin triggers reserpine-sensitive positive inotropic effect in perfused rat heart. PLoS ONE, 10(9), e0139208.CrossRef Gabrielová, E., Zholobenko, A. V., Bartošíková, L., Nečas, J., & Modriansky, M. (2015). Silymarin constituent 2,3-dehydrosilybin triggers reserpine-sensitive positive inotropic effect in perfused rat heart. PLoS ONE, 10(9), e0139208.CrossRef
16.
go back to reference Gharagozloo, M., Jafari, S., Esmaeil, N., Javid, E. N., Bagherpour, B., & Rezaei, A. (2013). Immunosuppressive effect of silymarin on mitogen-activated protein kinase signalling pathway: The impact on T cell proliferation and cytokine production. Basic & Clinical Pharmacology & Toxicology, 113, 209–214.CrossRef Gharagozloo, M., Jafari, S., Esmaeil, N., Javid, E. N., Bagherpour, B., & Rezaei, A. (2013). Immunosuppressive effect of silymarin on mitogen-activated protein kinase signalling pathway: The impact on T cell proliferation and cytokine production. Basic & Clinical Pharmacology & Toxicology, 113, 209–214.CrossRef
17.
go back to reference Goyal, B. R., & Mehta, A. A. (2012). Beneficial role of spironolactone, telmisartan and their combination on isoproterenol induced cardiac hypertrophy. Acta Cardiologica, 67, 203–211.CrossRef Goyal, B. R., & Mehta, A. A. (2012). Beneficial role of spironolactone, telmisartan and their combination on isoproterenol induced cardiac hypertrophy. Acta Cardiologica, 67, 203–211.CrossRef
18.
go back to reference Goyal, B. R., & Mehta, A. A. (2013). Diabetic cardiomyopathy: Pathophysiological mechanisms and cardiac dysfunction. Human & Experimental Toxicology, 32, 571–590.CrossRef Goyal, B. R., & Mehta, A. A. (2013). Diabetic cardiomyopathy: Pathophysiological mechanisms and cardiac dysfunction. Human & Experimental Toxicology, 32, 571–590.CrossRef
19.
go back to reference Goyal, B. R., Mesariya, P., Goyal, R. K., & Mehta, A. A. (2008). Effect of telmisartan on cardiovascular complications associated with streptozotocin diabetic rats. Molecular and Cellular Biochemistry, 314, 123–131.CrossRef Goyal, B. R., Mesariya, P., Goyal, R. K., & Mehta, A. A. (2008). Effect of telmisartan on cardiovascular complications associated with streptozotocin diabetic rats. Molecular and Cellular Biochemistry, 314, 123–131.CrossRef
20.
go back to reference Goyal, B. R., Parmar, K., Goyal, R. K., & Mehta, A. A. (2011). Beneficial role of telmisartan on cardiovascular complications associated with STZ-induced type-2 diabetic rats. Pharmacological Reports, 63, 956–966.CrossRef Goyal, B. R., Parmar, K., Goyal, R. K., & Mehta, A. A. (2011). Beneficial role of telmisartan on cardiovascular complications associated with STZ-induced type-2 diabetic rats. Pharmacological Reports, 63, 956–966.CrossRef
21.
go back to reference Goyal, B. R., Patel, M. M., & Bhadada, S. V. (2011). Comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril on diabetes induced cardiovascular complications in type 1 diabetes in rats. International Journal of Diabetes and Metabolism, 19, 11–18. Goyal, B. R., Patel, M. M., & Bhadada, S. V. (2011). Comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril on diabetes induced cardiovascular complications in type 1 diabetes in rats. International Journal of Diabetes and Metabolism, 19, 11–18.
22.
go back to reference Goyal, B. R., Solanki, N., Goyal, R. K., & Mehta, A. A. (2009). Investigation into the cardiac effects of spironolactone in the experimental model of type 1 diabetes. Journal of Cardiovascular Pharmacology, 54, 502–509.CrossRef Goyal, B. R., Solanki, N., Goyal, R. K., & Mehta, A. A. (2009). Investigation into the cardiac effects of spironolactone in the experimental model of type 1 diabetes. Journal of Cardiovascular Pharmacology, 54, 502–509.CrossRef
23.
go back to reference Hakan, A. Y., Arsava, M., & Okay, S. (2002). Creatine kinase-MB elevation after stroke is not cardiac in origin. Stroke 33, 286–290. Hakan, A. Y., Arsava, M., & Okay, S. (2002). Creatine kinase-MB elevation after stroke is not cardiac in origin. Stroke 33, 286–290.
24.
go back to reference Horton, J. W., Tan, J., White, J., & Maass, D. (2007). Burn injury decreases myocardial Na- K-ATPase activity: Role of PKC inhibition. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, R1684–R1692.CrossRef Horton, J. W., Tan, J., White, J., & Maass, D. (2007). Burn injury decreases myocardial Na- K-ATPase activity: Role of PKC inhibition. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, R1684–R1692.CrossRef
25.
go back to reference Huang, Q., Wu, L. J., Tashiro, S., Onodera, S., Li, L. H., & Ikejima, T. (2005). Silymarin augments human cervical cancer HeLa cell apoptosis via P38/JNK MAPK pathways in serum-free medium. Journal of Asian Natural Products Research, 7(5), 701–709.CrossRef Huang, Q., Wu, L. J., Tashiro, S., Onodera, S., Li, L. H., & Ikejima, T. (2005). Silymarin augments human cervical cancer HeLa cell apoptosis via P38/JNK MAPK pathways in serum-free medium. Journal of Asian Natural Products Research, 7(5), 701–709.CrossRef
26.
go back to reference Karamanlidis, G., Bautista-Hernandez, V., Fynn-Thompson, F., Del Nido, P., & Tian, R. (2011). Impaired mitochondrial biogenesis precedes heart failure in right ventricular hypertrophy in congenital heart disease. Circulation: Heart Failure, 4, 707–713. Karamanlidis, G., Bautista-Hernandez, V., Fynn-Thompson, F., Del Nido, P., & Tian, R. (2011). Impaired mitochondrial biogenesis precedes heart failure in right ventricular hypertrophy in congenital heart disease. Circulation: Heart Failure, 4, 707–713.
28.
go back to reference Kumphune, S., Chattipakorn, S., & Chattipakorn, N. (2012). Role of p38 inhibition in cardiac ischemia/reperfusion injury. European Journal of Clinical Pharmacology, 68, 513–524.CrossRef Kumphune, S., Chattipakorn, S., & Chattipakorn, N. (2012). Role of p38 inhibition in cardiac ischemia/reperfusion injury. European Journal of Clinical Pharmacology, 68, 513–524.CrossRef
29.
go back to reference Lee, J. K., & Kim, N. J. (2017). Recent advances in the inhibition of p38 MAPK as a potential strategy for the treatment of Alzheimer’s disease. Molecules, 22(8), E1287.CrossRef Lee, J. K., & Kim, N. J. (2017). Recent advances in the inhibition of p38 MAPK as a potential strategy for the treatment of Alzheimer’s disease. Molecules, 22(8), E1287.CrossRef
31.
go back to reference Molkentin, J. D., & Dorn, G. W. (2001). Cytoplasmic signaling pathways that regulate cardiac hypertrophy. Annual Review of Physiology, 63, 391–426.CrossRef Molkentin, J. D., & Dorn, G. W. (2001). Cytoplasmic signaling pathways that regulate cardiac hypertrophy. Annual Review of Physiology, 63, 391–426.CrossRef
32.
go back to reference Patel, B. M. (2018). Sodium butyrate controls cardiac hypertrophy in experimental models of rats. Cardiovascular Toxicology, 18(1), 1–8.CrossRef Patel, B. M. (2018). Sodium butyrate controls cardiac hypertrophy in experimental models of rats. Cardiovascular Toxicology, 18(1), 1–8.CrossRef
33.
go back to reference Patel, B. M., Agarwal, S. S., & Bhadada, S. V. (2012). Perindopril protects against streptozotocin induced hyperglycemic myocardial damage/alterations. Human & Experimental Toxicology, 31(11), 1138–1149.CrossRef Patel, B. M., Agarwal, S. S., & Bhadada, S. V. (2012). Perindopril protects against streptozotocin induced hyperglycemic myocardial damage/alterations. Human & Experimental Toxicology, 31(11), 1138–1149.CrossRef
34.
go back to reference Patel, B. M., & Desai, V. J. (2014). Beneficial role of tamoxifen in experimentally induced cardiac hypertrophy. Pharmacological Reports, 66, 264–272.CrossRef Patel, B. M., & Desai, V. J. (2014). Beneficial role of tamoxifen in experimentally induced cardiac hypertrophy. Pharmacological Reports, 66, 264–272.CrossRef
35.
go back to reference Patel, B. M., & Bhadada, S. V. (2014). Type 2 diabetes induced cardiovascular complications: Comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril. Clinical and Experimental Hypertension, 36, 340–347.CrossRef Patel, B. M., & Bhadada, S. V. (2014). Type 2 diabetes induced cardiovascular complications: Comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril. Clinical and Experimental Hypertension, 36, 340–347.CrossRef
36.
go back to reference Patel, B. M., Kakadiya, J., Goyal, R. K., & Mehta, A. A. (2013). Effect of spironolactone on cardiovascular complications associated with type-2 diabetes in rats. Experimental and Clinical Endocrinology, 121, 441–447.CrossRef Patel, B. M., Kakadiya, J., Goyal, R. K., & Mehta, A. A. (2013). Effect of spironolactone on cardiovascular complications associated with type-2 diabetes in rats. Experimental and Clinical Endocrinology, 121, 441–447.CrossRef
37.
go back to reference Patel, B. M., Mehta, A. A. (2013). The choice of anti-hypertensive agents in diabetic subjects. Diabetes and Vascular Disease Research, 10, 385–396.CrossRef Patel, B. M., Mehta, A. A. (2013). The choice of anti-hypertensive agents in diabetic subjects. Diabetes and Vascular Disease Research, 10, 385–396.CrossRef
38.
go back to reference Patel, B. M., & Mehta, A. A. (2012). Aldosterone and angiotensin: Role in diabetes and cardiovascular diseases. European Journal of Pharmacology, 697, 1–12.CrossRef Patel, B. M., & Mehta, A. A. (2012). Aldosterone and angiotensin: Role in diabetes and cardiovascular diseases. European Journal of Pharmacology, 697, 1–12.CrossRef
39.
go back to reference Patel, B. M., Raghunathan, S., & Porwal, U. (2014). Cardioprotective effects of magnesium valproate in type 2 diabetes mellitus. European Journal of Pharmacology, 728, 128–134.CrossRef Patel, B. M., Raghunathan, S., & Porwal, U. (2014). Cardioprotective effects of magnesium valproate in type 2 diabetes mellitus. European Journal of Pharmacology, 728, 128–134.CrossRef
40.
go back to reference Peppers, V., Ramos, G., Manias, E., Koroboki, E., Rokas, S., & Zakopoulos, N. (2008). Correlation between myocardial enzyme serum levels and markers of inflammation with severity of coronary artery disease and Gensini score: A hospital-based prospective study in Greek patients. Clinical Interventions in Aging, 3, 699–710.CrossRef Peppers, V., Ramos, G., Manias, E., Koroboki, E., Rokas, S., & Zakopoulos, N. (2008). Correlation between myocardial enzyme serum levels and markers of inflammation with severity of coronary artery disease and Gensini score: A hospital-based prospective study in Greek patients. Clinical Interventions in Aging, 3, 699–710.CrossRef
41.
go back to reference Post-White, J., Ladas, E. J., & Kelly, K. M. (2007). Advances in the use of milk thistle (Silybum marianum). Integrative Cancer Therapies, 6, 104–109.CrossRef Post-White, J., Ladas, E. J., & Kelly, K. M. (2007). Advances in the use of milk thistle (Silybum marianum). Integrative Cancer Therapies, 6, 104–109.CrossRef
42.
go back to reference Prockop, D. J., & Udenfriend, S. (1960). A specific method for the analysis of hydroxyproline in tissues and urine. Analytical Biochemistry, 1, 228–239.CrossRef Prockop, D. J., & Udenfriend, S. (1960). A specific method for the analysis of hydroxyproline in tissues and urine. Analytical Biochemistry, 1, 228–239.CrossRef
43.
go back to reference Raghunathan, S., & Patel, B. M. (2013). Therapeutic implications of small interfering RNA in cardiovascular diseases. Fundamental and Clinical Pharmacology, 27, 1–20.CrossRef Raghunathan, S., & Patel, B. M. (2013). Therapeutic implications of small interfering RNA in cardiovascular diseases. Fundamental and Clinical Pharmacology, 27, 1–20.CrossRef
44.
go back to reference Rao, P. R., & Viswanath, R. K. (2007). Cardioprotective activity of silymarin in ischemia-reperfusion-induced myocardial infarction in albino rats. Experimental & Clinical Cardiology, 12, 179–187. Rao, P. R., & Viswanath, R. K. (2007). Cardioprotective activity of silymarin in ischemia-reperfusion-induced myocardial infarction in albino rats. Experimental & Clinical Cardiology, 12, 179–187.
45.
go back to reference Rayabarapu, N., & Patel, B. M. (2014). Beneficial role of tamoxifen in isoproterenol induced myocardial infarction. Canadian Journal of Physiology and Pharmacology, 92, 849–857.CrossRef Rayabarapu, N., & Patel, B. M. (2014). Beneficial role of tamoxifen in isoproterenol induced myocardial infarction. Canadian Journal of Physiology and Pharmacology, 92, 849–857.CrossRef
46.
go back to reference Rosca, M. G., Tandler, B., & Hoppel, C. L. (2013). Mitochondria in cardiac hypertrophy and heart failure. Journal of Molecular and Cellular Cardiology, 55, 31–41.CrossRef Rosca, M. G., Tandler, B., & Hoppel, C. L. (2013). Mitochondria in cardiac hypertrophy and heart failure. Journal of Molecular and Cellular Cardiology, 55, 31–41.CrossRef
47.
go back to reference Rose, B. A., Force, T., & Wang, Y. (2010). Mitogen-activated protein kinase signaling in the heart: Angels versus demons in a heart-breaking tale. Physiological Reviews, 90, 1507–1546.CrossRef Rose, B. A., Force, T., & Wang, Y. (2010). Mitogen-activated protein kinase signaling in the heart: Angels versus demons in a heart-breaking tale. Physiological Reviews, 90, 1507–1546.CrossRef
48.
go back to reference Sakottova, N., Vecera, R., Urbenek, K., Vana, P., Walterova, D., & Cvak, L. (2003). Effects of polyphenolic fraction of silymarin on lipoprotein profile in rats fed cholesterol-rich diets. Pharmacological Research, 47, 17–26.CrossRef Sakottova, N., Vecera, R., Urbenek, K., Vana, P., Walterova, D., & Cvak, L. (2003). Effects of polyphenolic fraction of silymarin on lipoprotein profile in rats fed cholesterol-rich diets. Pharmacological Research, 47, 17–26.CrossRef
49.
go back to reference Sanz-Moreno, V., & Crespo, P. (2003). p38 mitogen-activated protein kinases: Their role in carcinogenesis. Revista de oncología, 5, 320–330. Sanz-Moreno, V., & Crespo, P. (2003). p38 mitogen-activated protein kinases: Their role in carcinogenesis. Revista de oncología, 5, 320–330.
50.
go back to reference Thakare, V. N., Aswar, M. K., Kulkarni, Y. P., Patil, R. R., & Patel, B. M. (2017). Silymarin ameliorates experimentally induced depressive like behavior in rats: Involvement of hippocampal BDNF signaling, inflammatory cytokines and oxidative stress response. Physiology & Behavior, 179, 401–410.CrossRef Thakare, V. N., Aswar, M. K., Kulkarni, Y. P., Patil, R. R., & Patel, B. M. (2017). Silymarin ameliorates experimentally induced depressive like behavior in rats: Involvement of hippocampal BDNF signaling, inflammatory cytokines and oxidative stress response. Physiology & Behavior, 179, 401–410.CrossRef
51.
go back to reference Thakare, V. N., Dhakane, V. D., & Patel, B. M. (2016). Potential antidepressant-like activity of silymarin in the acute restraint stress in mice: Modulation of corticosterone and oxidative stress response in cerebral cortex and hippocampus. Pharmacological Reports, 68, 1020–1027.CrossRef Thakare, V. N., Dhakane, V. D., & Patel, B. M. (2016). Potential antidepressant-like activity of silymarin in the acute restraint stress in mice: Modulation of corticosterone and oxidative stress response in cerebral cortex and hippocampus. Pharmacological Reports, 68, 1020–1027.CrossRef
52.
go back to reference Thakare, V. N., Patil, R. R., Oswal, R. J., Dhakane, V. D., Aswar, M. K., & Patel, B. M. (2018). Therapeutic potential of silymarin in chronic unpredictable mild stress induced depressive-like behavior in mice. Journal of Psychopharmacology, 32, 223–235.CrossRef Thakare, V. N., Patil, R. R., Oswal, R. J., Dhakane, V. D., Aswar, M. K., & Patel, B. M. (2018). Therapeutic potential of silymarin in chronic unpredictable mild stress induced depressive-like behavior in mice. Journal of Psychopharmacology, 32, 223–235.CrossRef
53.
go back to reference Tsimaratos, M., Coste, T. C., Djemli-Shipkolye, A., Daniel, L., Shipkolye, F., Vague, P., & Raccah, D. (2001). Evidence of time-dependent changes in renal medullary Na,K-ATPase activity and expression in diabetic rats. Cellular Molecular Biology (Noisy-le-grand), 47, 239–245. Tsimaratos, M., Coste, T. C., Djemli-Shipkolye, A., Daniel, L., Shipkolye, F., Vague, P., & Raccah, D. (2001). Evidence of time-dependent changes in renal medullary Na,K-ATPase activity and expression in diabetic rats. Cellular Molecular Biology (Noisy-le-grand), 47, 239–245.
54.
go back to reference Tuorkey, M. J., El-Desouki, N. I., & Kamel, R. A. (2015). Cytoprotective effect of Silymarin against diabetes-induced cardiomyocyte apoptosis in diabetic rats. Biomedical and Environmental Sciences, 28(1), 36–43.PubMed Tuorkey, M. J., El-Desouki, N. I., & Kamel, R. A. (2015). Cytoprotective effect of Silymarin against diabetes-induced cardiomyocyte apoptosis in diabetic rats. Biomedical and Environmental Sciences, 28(1), 36–43.PubMed
55.
go back to reference Wang, Y., Huang, S., Sah, V. P., Ross, J., Brown, J. H., Han, J., & Chien, K. R. (1998). Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. Journal of Biological Chemistry, 273, 2161–2168.CrossRef Wang, Y., Huang, S., Sah, V. P., Ross, J., Brown, J. H., Han, J., & Chien, K. R. (1998). Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. Journal of Biological Chemistry, 273, 2161–2168.CrossRef
56.
go back to reference Wu, J. H., Hagaman, J., Kim, S., Reddick, R. L., & Maeda, N. (2002). Aortic constriction exacerbates atherosclerosis and induces cardiac dysfunction in mice lacking apolipoprotein E. Arteriosclerosis, Thrombosis, and Vascular Biology, 22(3), 469–475.CrossRef Wu, J. H., Hagaman, J., Kim, S., Reddick, R. L., & Maeda, N. (2002). Aortic constriction exacerbates atherosclerosis and induces cardiac dysfunction in mice lacking apolipoprotein E. Arteriosclerosis, Thrombosis, and Vascular Biology, 22(3), 469–475.CrossRef
57.
go back to reference Zhang, S., Weinheimer, C., Courtois, M., Kovacs, A., Zhang, C. E., Cheng, A. M., Wang, Y., & Muslin, A. J. (2003). The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis. Journal of Clinical Investigation, 111, 833–841.CrossRef Zhang, S., Weinheimer, C., Courtois, M., Kovacs, A., Zhang, C. E., Cheng, A. M., Wang, Y., & Muslin, A. J. (2003). The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis. Journal of Clinical Investigation, 111, 833–841.CrossRef
58.
go back to reference Zholobenko, A., & Modriansky, M. (2014). Silymarin and its constituents in cardiac preconditioning. Fitoterapia, 97, 122–132.CrossRef Zholobenko, A., & Modriansky, M. (2014). Silymarin and its constituents in cardiac preconditioning. Fitoterapia, 97, 122–132.CrossRef
59.
go back to reference Zhou, B., Wu, L. J., Tashiro, S., Onodera, S., Uchiumi, F., & Ikejima, T. (2007). Activation of extracellular signal-regulated kinase during silibinin-protected, isoproterenol-induced apoptosis in rat cardiac myocytes is tyrosine kinase pathway-mediated and protein kinase C-dependent. Acta Pharmacologica Sinica, 28(6), 803–810.CrossRef Zhou, B., Wu, L. J., Tashiro, S., Onodera, S., Uchiumi, F., & Ikejima, T. (2007). Activation of extracellular signal-regulated kinase during silibinin-protected, isoproterenol-induced apoptosis in rat cardiac myocytes is tyrosine kinase pathway-mediated and protein kinase C-dependent. Acta Pharmacologica Sinica, 28(6), 803–810.CrossRef
Metadata
Title
Beneficial Effect of Silymarin in Pressure Overload Induced Experimental Cardiac Hypertrophy
Authors
Basant Sharma
Udit Chaube
Bhoomika M. Patel
Publication date
01-02-2019
Publisher
Springer US
Published in
Cardiovascular Toxicology / Issue 1/2019
Print ISSN: 1530-7905
Electronic ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-018-9470-2

Other articles of this Issue 1/2019

Cardiovascular Toxicology 1/2019 Go to the issue