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Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H2O2-Induced HUVECs.
Liao, Li; Gong, Lihong; Zhou, Mengting; Xue, Xinyan; Li, Yunxia; Peng, Cheng.
  • Liao L; State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu 611137, China.
  • Gong L; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
  • Zhou M; National Key Laboratory Breeding Base of Systematic Research, Development and Utilization of Chinese Medicine Resources, Chengdu 611137, China.
  • Xue X; State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu 611137, China.
  • Li Y; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
  • Peng C; National Key Laboratory Breeding Base of Systematic Research, Development and Utilization of Chinese Medicine Resources, Chengdu 611137, China.
Oxid Med Cell Longev ; 2021: 9919466, 2021.
Article in English | MEDLINE | ID: covidwho-1358940
ABSTRACT
Thrombus is considered to be the pathological source of morbidity and mortality of cardiovascular disease and thrombotic complications, while oxidative stress is regarded as an important factor in vascular endothelial injury and thrombus formation. Therefore, antioxidative stress and maintaining the normal function of vascular endothelial cells are greatly significant in regulating vascular tension and maintaining a nonthrombotic environment. Leonurine (LEO) is a unique alkaloid isolated from Leonurus japonicus Houtt (a traditional Chinese medicine (TCM)), which has shown a good effect on promoting blood circulation and removing blood stasis. In this study, we explored the protective effect and action mechanism of LEO on human umbilical vein endothelial cells (HUVECs) after damage by hydrogen peroxide (H2O2). The protective effects of LEO on H2O2-induced HUVECs were determined by measuring the cell viability, cell migration, tube formation, and oxidative biomarkers. The underlying mechanism of antioxidation of LEO was investigated by RT-qPCR and western blotting. Our results showed that LEO treatment promoted cell viability; remarkably downregulated the intracellular generation of reactive oxygen species (ROS), malondialdehyde (MDA) production, and lactate dehydrogenase (LDH); and upregulated the nitric oxide (NO) and superoxide dismutase (SOD) activity in H2O2-induced HUVECs. At the same time, LEO treatment significantly promoted the phosphorylation level of angiogenic protein PI3K, Akt, and eNOS and the expression level of survival factor Bcl2 and decreased the expression level of death factor Bax and caspase3. In conclusion, our findings suggested that LEO can ameliorate the oxidative stress damage and insufficient angiogenesis of HUVECs induced by H2O2 through activating the PI3K/Akt-eNOS signaling pathway.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Signal Transduction / Oxidative Stress / Gallic Acid Type of study: Diagnostic study Topics: Traditional medicine Limits: Humans Language: English Journal: Oxid Med Cell Longev Journal subject: Metabolism Year: 2021 Document Type: Article Affiliation country: 2021

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Signal Transduction / Oxidative Stress / Gallic Acid Type of study: Diagnostic study Topics: Traditional medicine Limits: Humans Language: English Journal: Oxid Med Cell Longev Journal subject: Metabolism Year: 2021 Document Type: Article Affiliation country: 2021