Protective effects of magnesium lithospermate B against diabetic atherosclerosis via Nrf2-ARE-NQO1 transcriptional pathway
Abstract Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including atherosclerosis. Although a number of antioxidants are available, none have been found to be suitable for regulating the oxidative stress response and en...
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Published in | Atherosclerosis Vol. 211; no. 1; pp. 69 - 76 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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01.07.2010
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Abstract | Abstract Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including atherosclerosis. Although a number of antioxidants are available, none have been found to be suitable for regulating the oxidative stress response and enhancing antioxidative defense mechanisms. In this study, we evaluated the effects of magnesium lithospermate B (LAB) against oxidative stress. We also endeavored to identify the target molecule of LAB in vascular smooth muscle cells (VSMCs) and the underlying biochemical pathways related to diabetic atherosclerosis. Modified MTT and transwell assays showed that the increased proliferation and migration of rat aortic VSMCs in culture with high glucose was significantly inhibited by LAB. LAB also attenuated neointimal hyperplasia after balloon catheter injury in diabetic rat carotid arteries. To determine molecular targets of LAB, we studied the effects of LAB on aldose reductase (AR) activity, O-GlcNAcylation, and protein kinase C (PKC) activity in VSMCs under normoglycemic or hyperglycemic conditions and showed the improvement of major biochemical pathways by LAB. Potential involvement of the nuclear factor erythroid 2-related factor-2 (Nrf2) – antioxidant responsive element (ARE)-NAD(P)H: quinone oxidoreductase-1 (NQO1) pathway was assessed using siRNA methods. We found that LAB activates the NQO1 via the Nrf2-ARE pathway, which plays an important role in inhibition of the major molecular mechanisms that lead to vascular damage and the proliferation and migration of VSMCs. Together, these findings demonstrate that the induction of the Nrf2-ARE-NQO1 pathway by LAB could be a new therapeutic strategy to prevent diabetic atherosclerosis. |
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AbstractList | Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including atherosclerosis. Although a number of antioxidants are available, none have been found to be suitable for regulating the oxidative stress response and enhancing antioxidative defense mechanisms. In this study, we evaluated the effects of magnesium lithospermate B (LAB) against oxidative stress. We also endeavored to identify the target molecule of LAB in vascular smooth muscle cells (VSMCs) and the underlying biochemical pathways related to diabetic atherosclerosis. Modified MTT and transwell assays showed that the increased proliferation and migration of rat aortic VSMCs in culture with high glucose was significantly inhibited by LAB. LAB also attenuated neointimal hyperplasia after balloon catheter injury in diabetic rat carotid arteries. To determine molecular targets of LAB, we studied the effects of LAB on aldose reductase (AR) activity, O-GlcNAcylation, and protein kinase C (PKC) activity in VSMCs under normoglycemic or hyperglycemic conditions and showed the improvement of major biochemical pathways by LAB. Potential involvement of the nuclear factor erythroid 2-related factor-2 (Nrf2)--antioxidant responsive element (ARE)-NAD(P)H: quinone oxidoreductase-1 (NQO1) pathway was assessed using siRNA methods. We found that LAB activates the NQO1 via the Nrf2-ARE pathway, which plays an important role in inhibition of the major molecular mechanisms that lead to vascular damage and the proliferation and migration of VSMCs. Together, these findings demonstrate that the induction of the Nrf2-ARE-NQO1 pathway by LAB could be a new therapeutic strategy to prevent diabetic atherosclerosis. Abstract Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including atherosclerosis. Although a number of antioxidants are available, none have been found to be suitable for regulating the oxidative stress response and enhancing antioxidative defense mechanisms. In this study, we evaluated the effects of magnesium lithospermate B (LAB) against oxidative stress. We also endeavored to identify the target molecule of LAB in vascular smooth muscle cells (VSMCs) and the underlying biochemical pathways related to diabetic atherosclerosis. Modified MTT and transwell assays showed that the increased proliferation and migration of rat aortic VSMCs in culture with high glucose was significantly inhibited by LAB. LAB also attenuated neointimal hyperplasia after balloon catheter injury in diabetic rat carotid arteries. To determine molecular targets of LAB, we studied the effects of LAB on aldose reductase (AR) activity, O-GlcNAcylation, and protein kinase C (PKC) activity in VSMCs under normoglycemic or hyperglycemic conditions and showed the improvement of major biochemical pathways by LAB. Potential involvement of the nuclear factor erythroid 2-related factor-2 (Nrf2) – antioxidant responsive element (ARE)-NAD(P)H: quinone oxidoreductase-1 (NQO1) pathway was assessed using siRNA methods. We found that LAB activates the NQO1 via the Nrf2-ARE pathway, which plays an important role in inhibition of the major molecular mechanisms that lead to vascular damage and the proliferation and migration of VSMCs. Together, these findings demonstrate that the induction of the Nrf2-ARE-NQO1 pathway by LAB could be a new therapeutic strategy to prevent diabetic atherosclerosis. |
Author | Lee, Yong-ho Lee, Hyun Chul Lee, Eun Jig Kim, Soo Hyun Jung, Mankil Hur, Kyu Yeon Yadav, Umesh C.S Williams, Darren R Kang, Sang Won Srivastava, Satish K Cho, Jin Won Kim, Sang Geon Kang, Eun Seok Choi, Min-Ah |
Author_xml | – sequence: 1 fullname: Hur, Kyu Yeon – sequence: 2 fullname: Kim, Soo Hyun – sequence: 3 fullname: Choi, Min-Ah – sequence: 4 fullname: Williams, Darren R – sequence: 5 fullname: Lee, Yong-ho – sequence: 6 fullname: Kang, Sang Won – sequence: 7 fullname: Yadav, Umesh C.S – sequence: 8 fullname: Srivastava, Satish K – sequence: 9 fullname: Jung, Mankil – sequence: 10 fullname: Cho, Jin Won – sequence: 11 fullname: Kim, Sang Geon – sequence: 12 fullname: Kang, Eun Seok – sequence: 13 fullname: Lee, Eun Jig – sequence: 14 fullname: Lee, Hyun Chul |
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Keywords | Magnesium lithospermate B Oxidative stress Nrf2 Diabetes mellitus Diabetic atherosclerosis Endocrinopathy Vascular disease Prevention Atherosclerosis Cardiovascular disease Magnesium Inorganic element |
Language | English |
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Snippet | Abstract Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including... Hyperglycemia-induced oxidative stress is known to play an important role in the development of several diabetic complications, including atherosclerosis.... |
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SubjectTerms | Aldehyde Reductase - metabolism Animals Antioxidants - pharmacology Associated diseases and complications Atherosclerosis (general aspects, experimental research) Atherosclerosis - metabolism Atherosclerosis - prevention & control Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular Diabetes mellitus Diabetes Mellitus, Experimental - complications Diabetes. Impaired glucose tolerance Diabetic atherosclerosis Drugs, Chinese Herbal - therapeutic use Endocrine pancreas. Apud cells (diseases) Endocrinopathies Magnesium lithospermate B Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism NAD(P)H Dehydrogenase (Quinone) - physiology NF-E2-Related Factor 2 - physiology Nrf2 Oxidative stress Oxidative Stress - drug effects Protein Kinase C - metabolism Rats Rats, Sprague-Dawley Response Elements - physiology |
Title | Protective effects of magnesium lithospermate B against diabetic atherosclerosis via Nrf2-ARE-NQO1 transcriptional pathway |
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