16 results on '"Qi Zhu"'
Search Results
2. Piperine Alleviates Doxorubicin-Induced Cardiotoxicity via Activating PPAR
- Author
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Jie, Yan, Si-Chi, Xu, Chun-Yan, Kong, Xiao-Yang, Zhou, Zhou-Yan, Bian, Ling, Yan, and Qi-Zhu, Tang
- Subjects
carbohydrates (lipids) ,polycyclic compounds ,Research Article - Abstract
Background Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice. Methods To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection. Results Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ), and the protective effects of piperine were abolished by the treatment of the PPAR-γ antagonist in vivo and in vitro. Conclusions Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice.
- Published
- 2019
3. Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3βand MAPK Signaling Pathways
- Author
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Si-Chi Xu, Zhen-Guo Ma, Ning Zhang, Qi-Zhu Tang, and Wen-Ying Wei
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,medicine.medical_specialty ,Article Subject ,Cardiac fibrosis ,Peroxisome proliferator-activated receptor ,Biology ,Muscle hypertrophy ,03 medical and health sciences ,Internal medicine ,Drug Discovery ,medicine ,Pharmacology (medical) ,Protein kinase A ,Glycogen synthase ,lcsh:QH301-705.5 ,Protein kinase B ,chemistry.chemical_classification ,medicine.disease ,030104 developmental biology ,Endocrinology ,lcsh:Biology (General) ,chemistry ,biology.protein ,Pioglitazone ,Research Article ,medicine.drug - Abstract
Peroxisome proliferator activated receptorγ(PPARγ) has been closely involved in the process of cardiovascular diseases. This study was to investigate whether pioglitazone (PIO), a PPARγagonist, could protect against pressure overload-induced cardiac hypertrophy. Mice were orally given PIO (2.5 mg/kg) from 1 week after aortic banding and continuing for 7 weeks. The morphological examination and biochemical analysis were used to evaluate the effects of PIO. Neonatal rat ventricular cardiomyocytes were also used to verify the protection of PIO against hypertrophy in vitro. The results in our study demonstrated that PIO remarkably inhibited hypertrophic response induced by aortic banding in vivo. Besides, PIO also suppressed cardiac fibrosis in vivo. PIO treatment also inhibited the activation of protein kinase B (AKT)/glycogen synthase kinase-3β(GSK3β) and mitogen-activated protein kinase (MAPK) in the heart. In addition, PIO alleviated angiotensin II-induced hypertrophic response in vitro. In conclusion, PIO could inhibit cardiac hypertrophy via attenuation of AKT/GSK3βand MAPK pathways.
- Published
- 2016
4. Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF
- Author
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Ya-Ge, Jin, Yuan, Yuan, Qing-Qing, Wu, Ning, Zhang, Di, Fan, Yan, Che, Zhao-Peng, Wang, Yang, Xiao, Sha-Sha, Wang, and Qi-Zhu, Tang
- Subjects
cardiovascular system ,Research Article - Abstract
Background Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-β1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-γ (PPAR-γ) were used to explore the underlying mechanism. Results Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-β1/Smad2 signaling pathway was blunted and PPAR-γ expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-γ and the inhibition of TGF-β1/Smad2-mediated EndMT.
- Published
- 2017
5. Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition
- Author
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Yuan Yuan, Ya-Ge Jin, Qi-Zhu Tang, Yan Che, Qing-Qing Wu, Ning Zhang, Zhao-Peng Wang, Yang Xiao, Sha-Sha Wang, and Di Fan
- Subjects
0301 basic medicine ,CD31 ,medicine.medical_specialty ,Article Subject ,Cardiac fibrosis ,Vimentin ,Umbilical vein ,03 medical and health sciences ,chemistry.chemical_compound ,Downregulation and upregulation ,Puerarin ,Internal medicine ,Drug Discovery ,medicine ,Pharmacology (medical) ,Receptor ,lcsh:QH301-705.5 ,biology ,business.industry ,medicine.disease ,030104 developmental biology ,Endocrinology ,chemistry ,lcsh:Biology (General) ,biology.protein ,cardiovascular system ,business ,Transforming growth factor - Abstract
Background. Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-β1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-γ (PPAR-γ) were used to explore the underlying mechanism. Results. Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-β1/Smad2 signaling pathway was blunted and PPAR-γ expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion. Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-γ and the inhibition of TGF-β1/Smad2-mediated EndMT.
- Published
- 2017
- Full Text
- View/download PDF
6. Peroxisome Proliferator-Activated Receptor-γ Is Critical to Cardiac Fibrosis
- Author
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Qi-Zhu Tang, Zheng Yang, Huang-Jun Liu, and Hai-Han Liao
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Cardiac fibrosis ,Ischemia ,Peroxisome proliferator-activated receptor ,Inflammation ,Review Article ,030204 cardiovascular system & hematology ,Pharmacology ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Drug Discovery ,Medicine ,Pharmacology (medical) ,Receptor ,lcsh:QH301-705.5 ,chemistry.chemical_classification ,business.industry ,medicine.disease ,030104 developmental biology ,Endocrinology ,chemistry ,Nuclear receptor ,lcsh:Biology (General) ,Heart failure ,medicine.symptom ,business ,Reperfusion injury - Abstract
Peroxisome proliferator-activated receptor-γ(PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγagonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγin various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγagonists for the clinical management of CVD.
- Published
- 2016
7. Peroxisome Proliferator-Activated Receptor-γ Is Critical to Cardiac Fibrosis
- Author
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Liu, Huang-Jun, Liao, Hai-Han, Yang, Zheng, and Tang, Qi-Zhu
- Subjects
Article Subject - Abstract
Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγ agonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγ in various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγ agonists for the clinical management of CVD.
- Published
- 2016
- Full Text
- View/download PDF
8. Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis
- Author
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Xu, Si-Chi, primary, Ma, Zhen-Guo, additional, Wei, Wen-Ying, additional, Yuan, Yu-Pei, additional, and Tang, Qi-Zhu, additional
- Published
- 2017
- Full Text
- View/download PDF
9. Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition
- Author
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Jin, Ya-Ge, primary, Yuan, Yuan, additional, Wu, Qing-Qing, additional, Zhang, Ning, additional, Fan, Di, additional, Che, Yan, additional, Wang, Zhao-Peng, additional, Xiao, Yang, additional, Wang, Sha-Sha, additional, and Tang, Qi-Zhu, additional
- Published
- 2017
- Full Text
- View/download PDF
10. Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3βand MAPK Signaling Pathways
- Author
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Wei, Wen-Ying, primary, Ma, Zhen-Guo, additional, Xu, Si-Chi, additional, Zhang, Ning, additional, and Tang, Qi-Zhu, additional
- Published
- 2016
- Full Text
- View/download PDF
11. Peroxisome Proliferator-Activated Receptor-γIs Critical to Cardiac Fibrosis
- Author
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Liu, Huang-Jun, primary, Liao, Hai-Han, additional, Yang, Zheng, additional, and Tang, Qi-Zhu, additional
- Published
- 2016
- Full Text
- View/download PDF
12. Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3β and MAPK Signaling Pathways.
- Author
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Wei, Wen-Ying, Ma, Zhen-Guo, Xu, Si-Chi, Zhang, Ning, and Tang, Qi-Zhu
- Subjects
PIOGLITAZONE ,HEART diseases ,THERAPEUTICS ,CARDIAC hypertrophy ,MITOGEN-activated protein kinases ,PEROXISOME proliferator-activated receptors ,PROTEIN kinase B ,GLYCOGEN synthase kinase ,IN vitro studies ,LABORATORY rats - Abstract
Peroxisome proliferator activated receptor γ (PPARγ) has been closely involved in the process of cardiovascular diseases. This study was to investigate whether pioglitazone (PIO), a PPARγ agonist, could protect against pressure overload-induced cardiac hypertrophy. Mice were orally given PIO (2.5 mg/kg) from 1 week after aortic banding and continuing for 7 weeks. The morphological examination and biochemical analysis were used to evaluate the effects of PIO. Neonatal rat ventricular cardiomyocytes were also used to verify the protection of PIO against hypertrophy in vitro. The results in our study demonstrated that PIO remarkably inhibited hypertrophic response induced by aortic banding in vivo. Besides, PIO also suppressed cardiac fibrosis in vivo. PIO treatment also inhibited the activation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinase (MAPK) in the heart. In addition, PIO alleviated angiotensin II-induced hypertrophic response in vitro. In conclusion, PIO could inhibit cardiac hypertrophy via attenuation of AKT/GSK3β and MAPK pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
13. Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis
- Author
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Si-Chi Xu, Zhen-Guo Ma, Wen-Ying Wei, Yu-Pei Yuan, and Qi-Zhu Tang
- Subjects
Biology (General) ,QH301-705.5 - Abstract
Background. Peroxisome proliferator-activated receptor-α (PPAR-α) is closely associated with the development of cardiac hypertrophy. Previous studies have indicated that bezafibrate (BZA), a PPAR-α agonist, could attenuate insulin resistance and obesity. This study was designed to determine whether BZA could protect against pressure overload-induced cardiac hypertrophy. Methods. Mice were orally given BZA (100 mg/kg) for 7 weeks beginning 1 week after aortic banding (AB) surgery. Cardiac hypertrophy was assessed based on echocardiographic, histological, and molecular aspects. Moreover, neonatal rat ventricular cardiomyocytes (NRVMs) were used to investigate the effects of BZA on the cardiomyocyte hypertrophic response in vitro. Results. Our study demonstrated that BZA could alleviate cardiac hypertrophy and fibrosis in mice subjected to AB surgery. BZA treatment also reduced the phosphorylation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinases (MAPKs). BZA suppressed phenylephrine- (PE-) induced hypertrophy of cardiomyocyte in vitro. The protective effects of BZA were abolished by the treatment of the PPAR-α antagonist in vitro. Conclusions. BZA could attenuate pressure overload-induced cardiac hypertrophy and fibrosis.
- Published
- 2017
- Full Text
- View/download PDF
14. Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3β and MAPK Signaling Pathways
- Author
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Wen-Ying Wei, Zhen-Guo Ma, Si-Chi Xu, Ning Zhang, and Qi-Zhu Tang
- Subjects
Biology (General) ,QH301-705.5 - Abstract
Peroxisome proliferator activated receptor γ (PPARγ) has been closely involved in the process of cardiovascular diseases. This study was to investigate whether pioglitazone (PIO), a PPARγ agonist, could protect against pressure overload-induced cardiac hypertrophy. Mice were orally given PIO (2.5 mg/kg) from 1 week after aortic banding and continuing for 7 weeks. The morphological examination and biochemical analysis were used to evaluate the effects of PIO. Neonatal rat ventricular cardiomyocytes were also used to verify the protection of PIO against hypertrophy in vitro. The results in our study demonstrated that PIO remarkably inhibited hypertrophic response induced by aortic banding in vivo. Besides, PIO also suppressed cardiac fibrosis in vivo. PIO treatment also inhibited the activation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinase (MAPK) in the heart. In addition, PIO alleviated angiotensin II-induced hypertrophic response in vitro. In conclusion, PIO could inhibit cardiac hypertrophy via attenuation of AKT/GSK3β and MAPK pathways.
- Published
- 2016
- Full Text
- View/download PDF
15. Peroxisome Proliferator-Activated Receptor-γ Is Critical to Cardiac Fibrosis
- Author
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Huang-Jun Liu, Hai-Han Liao, Zheng Yang, and Qi-Zhu Tang
- Subjects
Biology (General) ,QH301-705.5 - Abstract
Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγ agonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγ in various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγ agonists for the clinical management of CVD.
- Published
- 2016
- Full Text
- View/download PDF
16. Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF- β 1/Smad2-Mediated Endothelial-to-Mesenchymal Transition.
- Author
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Jin YG, Yuan Y, Wu QQ, Zhang N, Fan D, Che Y, Wang ZP, Xiao Y, Wang SS, and Tang QZ
- Abstract
Background: Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis., Methods: Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF- β 1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor- γ (PPAR- γ ) were used to explore the underlying mechanism., Results: Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF- β 1/Smad2 signaling pathway was blunted and PPAR- γ expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin., Conclusion: Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR- γ and the inhibition of TGF- β 1/Smad2-mediated EndMT.
- Published
- 2017
- Full Text
- View/download PDF
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