Tags

Type your tag names separated by a space and hit enter

Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stress.
Endocrine 2018; 60(1):83-94E

Abstract

PURPOSE

Suppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism.

METHODS

Anti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS. Streptozotocin (STZ)-induced type 1 diabetes mellitus mice were constructed. Corresponding to experiments in vitro, the therapeutic effect of KPF was also assessed using heart tissues from mice.

RESULTS

KPF significantly inhibited high glocose (HG) induced expression of inflammatory cytokines and generation of ROS, leading to reduced fibrotic responses and cell apoptosis in vitro. KPF mediated DCM protective effects through inhibiting nuclear factor-κB (NF-κB) nucleus translocation and activating nuclear factor-erythroid 2 p45-related factor-2 (Nrf-2). In STZ-induced type 1 diabetic mouse model, KPF prevented diabetes-induced cardiac fibrosis and apoptosis. These changes were also accompanied by reducing inflammation and oxidative stress in diabetic mice hearts.

CONCLUSION

KPF is a potential therapeutic agent for the treatment of DCM, mechanically linked to inhibition of NF-κB and Nrf-2 activation.

Authors+Show Affiliations

Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China. Department of Cardiology, The First Affiliated Hospital, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Department of Pathology and Laboratory Medicine, Western University, London, ON, N6A5C1, Canada.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China. jingyingwang0605@163.com.Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, Zhejiang, China. wzmcliangguang@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29392616

Citation

Chen, Xuemei, et al. "Kaempferol Attenuates Hyperglycemia-induced Cardiac Injuries By Inhibiting Inflammatory Responses and Oxidative Stress." Endocrine, vol. 60, no. 1, 2018, pp. 83-94.
Chen X, Qian J, Wang L, et al. Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stress. Endocrine. 2018;60(1):83-94.
Chen, X., Qian, J., Wang, L., Li, J., Zhao, Y., Han, J., ... Liang, G. (2018). Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stress. Endocrine, 60(1), pp. 83-94. doi:10.1007/s12020-018-1525-4.
Chen X, et al. Kaempferol Attenuates Hyperglycemia-induced Cardiac Injuries By Inhibiting Inflammatory Responses and Oxidative Stress. Endocrine. 2018;60(1):83-94. PubMed PMID: 29392616.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stress. AU - Chen,Xuemei, AU - Qian,Jianchang, AU - Wang,Lintao, AU - Li,Jieli, AU - Zhao,Yunjie, AU - Han,Jibo, AU - Khan,Zia, AU - Chen,Xiaojun, AU - Wang,Jingying, AU - Liang,Guang, Y1 - 2018/02/01/ PY - 2017/09/18/received PY - 2018/01/09/accepted PY - 2018/2/3/pubmed PY - 2018/10/26/medline PY - 2018/2/3/entrez KW - Diabetic cardiomyopathy KW - Inflammation KW - Kaempferol KW - NF-κB KW - Nrf-2 KW - Oxidative stress SP - 83 EP - 94 JF - Endocrine JO - Endocrine VL - 60 IS - 1 N2 - PURPOSE: Suppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism. METHODS: Anti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS. Streptozotocin (STZ)-induced type 1 diabetes mellitus mice were constructed. Corresponding to experiments in vitro, the therapeutic effect of KPF was also assessed using heart tissues from mice. RESULTS: KPF significantly inhibited high glocose (HG) induced expression of inflammatory cytokines and generation of ROS, leading to reduced fibrotic responses and cell apoptosis in vitro. KPF mediated DCM protective effects through inhibiting nuclear factor-κB (NF-κB) nucleus translocation and activating nuclear factor-erythroid 2 p45-related factor-2 (Nrf-2). In STZ-induced type 1 diabetic mouse model, KPF prevented diabetes-induced cardiac fibrosis and apoptosis. These changes were also accompanied by reducing inflammation and oxidative stress in diabetic mice hearts. CONCLUSION: KPF is a potential therapeutic agent for the treatment of DCM, mechanically linked to inhibition of NF-κB and Nrf-2 activation. SN - 1559-0100 UR - https://www.unboundmedicine.com/medline/citation/29392616/Kaempferol_attenuates_hyperglycemia_induced_cardiac_injuries_by_inhibiting_inflammatory_responses_and_oxidative_stress_ L2 - https://dx.doi.org/10.1007/s12020-018-1525-4 DB - PRIME DP - Unbound Medicine ER -