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Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
Published on: September 28, 2015
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Baicalin attenuates angiotensin II-induced endothelial dysfunction.
Xiling Wei1, Xingyu Zhu1, Nan Hu1
1School of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
Biochemical and Biophysical Research Communications
|August 5, 2015
Summary
Baicalin protects against Angiotensin II (Ang II) induced endothelial injury by reducing cell death and oxidative stress. It activates beneficial pathways, improving blood vessel function and offering cardiovascular protection.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Pharmacology
Background:
- Angiotensin II (Ang II) triggers pathways leading to endothelial dysfunction and oxidative stress.
- Baicalin, a natural flavone, demonstrates antioxidant and anti-apoptotic properties relevant to cardiovascular diseases.
Purpose of the Study:
- To investigate the protective effects of baicalin against Angiotensin II-induced injury in human umbilical vein endothelial cells (HUVECs).
Main Methods:
- Assessed endothelial function, apoptosis markers (Bax, Bcl-2, cleaved caspase-3), Angiotensin-converting enzyme 2 (ACE2)/Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, oxidative stress markers (MDA, ROS, NO, T-AOC), and the PI3K/AKT/eNOS pathway in HUVECs treated with Ang II and baicalin.
Main Results:
- Baicalin improved Ang II-impaired endothelial function, reduced HUVEC apoptosis, and increased the ratio of Bcl-2 to Bax and cleaved caspase-3.
- Baicalin promoted the conversion of Ang II to Ang-(1-7) by upregulating ACE2 and Mas receptor expression.
- Baicalin mitigated Ang II-induced oxidative damage by decreasing MDA and ROS, and increasing NO and T-AOC, linked to enhanced PI3K/AKT/eNOS signaling.
Conclusions:
- Baicalin protects endothelial cells from Ang II-induced dysfunction and oxidative stress.
- The protective mechanisms involve modulating apoptosis-related proteins, activating the ACE2/Ang-(1-7)/Mas axis, and upregulating the PI3K/AKT/eNOS pathway.
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