Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway
Background. Aloe emodin (AE) is a lipid-lowering agent, which could be used to treat hyperlipidemia, thereby reducing the risk of cardiovascular disease. Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages. Purpose...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/6318520 |
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| author | Yingfu Chen Burong Feng Ye Yuan Juan Hu Wei Zhao Huiwei Jiang Wen Li Ziyi Fan Zhimin Du |
| author_facet | Yingfu Chen Burong Feng Ye Yuan Juan Hu Wei Zhao Huiwei Jiang Wen Li Ziyi Fan Zhimin Du |
| author_sort | Yingfu Chen |
| collection | DOAJ |
| description | Background. Aloe emodin (AE) is a lipid-lowering agent, which could be used to treat hyperlipidemia, thereby reducing the risk of cardiovascular disease. Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages. Purpose. The purpose of this study is to evaluate the potential roles and mechanisms of AE in hyperlipidemia-induced oxidative stress and inflammation in the heart. Study Design. We established a hyperlipidemia-induced cardiac inflammation model in rats and cells then administered AE and observed its effect on hyperlipidemia-induced cardiac inflammation. Methods. We used a mouse model of hyperlipidemia caused by a high-fat diet (HFD) for 10 weeks and cell culture experimental models of inflammation in the heart stimulated by PA for 14 h. Inflammatory markers were detected by qRT-PCR, WB, and immunofluorescence. Results. We demonstrated that the expression levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. Our in vitro study showed AE treatment dose-dependently decreased the expression of IL-1β, IL-6, and TNF-α in PA-treated H9C2 cells. Further experiments revealed that AE inhibited PA-induced cell death and promoted the production of intracellular reactive oxygen species (ROS). Mechanically, AE significantly suppressed the upregulation in protein levels of TLR4, IκB, and p-P65l in vivo and in vitro. Conclusion. Taken together, our findings disclose that AE could alleviate HFD/PA-induced cardiac inflammation via inhibition of the TLR4/NF-κB signaling pathway. Thus, AE may be a promising therapeutic strategy for preventing hyperlipidemia-induced myocardial injury. |
| format | Article |
| id | doaj-art-7903a11f71924bf59be8630e07791dd5 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-7903a11f71924bf59be8630e07791dd52025-02-03T01:00:05ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/63185206318520Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling PathwayYingfu Chen0Burong Feng1Ye Yuan2Juan Hu3Wei Zhao4Huiwei Jiang5Wen Li6Ziyi Fan7Zhimin Du8Institute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaInstitute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University (The University Key Laboratory of Drug Research, Heilongjiang Province, Harbin 150086, ChinaBackground. Aloe emodin (AE) is a lipid-lowering agent, which could be used to treat hyperlipidemia, thereby reducing the risk of cardiovascular disease. Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages. Purpose. The purpose of this study is to evaluate the potential roles and mechanisms of AE in hyperlipidemia-induced oxidative stress and inflammation in the heart. Study Design. We established a hyperlipidemia-induced cardiac inflammation model in rats and cells then administered AE and observed its effect on hyperlipidemia-induced cardiac inflammation. Methods. We used a mouse model of hyperlipidemia caused by a high-fat diet (HFD) for 10 weeks and cell culture experimental models of inflammation in the heart stimulated by PA for 14 h. Inflammatory markers were detected by qRT-PCR, WB, and immunofluorescence. Results. We demonstrated that the expression levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. Our in vitro study showed AE treatment dose-dependently decreased the expression of IL-1β, IL-6, and TNF-α in PA-treated H9C2 cells. Further experiments revealed that AE inhibited PA-induced cell death and promoted the production of intracellular reactive oxygen species (ROS). Mechanically, AE significantly suppressed the upregulation in protein levels of TLR4, IκB, and p-P65l in vivo and in vitro. Conclusion. Taken together, our findings disclose that AE could alleviate HFD/PA-induced cardiac inflammation via inhibition of the TLR4/NF-κB signaling pathway. Thus, AE may be a promising therapeutic strategy for preventing hyperlipidemia-induced myocardial injury.http://dx.doi.org/10.1155/2020/6318520 |
| spellingShingle | Yingfu Chen Burong Feng Ye Yuan Juan Hu Wei Zhao Huiwei Jiang Wen Li Ziyi Fan Zhimin Du Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway Mediators of Inflammation |
| title | Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway |
| title_full | Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway |
| title_fullStr | Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway |
| title_full_unstemmed | Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway |
| title_short | Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway |
| title_sort | aloe emodin reduces cardiac inflammation induced by a high fat diet through the tlr4 signaling pathway |
| url | http://dx.doi.org/10.1155/2020/6318520 |
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