AI Article Synopsis
- Berberine (BBR) is a traditional Chinese medicine known for its anti-inflammatory and anti-oxidative properties, commonly used to treat hypertension, but its exact mechanism in the brain isn't well understood.
- This study investigates whether chronic BBR infusion in the hypothalamic paraventricular nucleus (PVN) can reduce high blood pressure and sympathetic nervous system activity through a specific signaling pathway.
- Results showed that BBR significantly lowers mean arterial pressure and related biochemical markers in hypertensive rats, indicating it works via the ROS/Erk1/2/iNOS pathway to combat hypertension.
Article Abstract
Background: Berberine (BBR), a Chinese traditional herbal medicine, has many pharmacologic benefits such as anti-inflammation and anti-oxidation. It is widely used in clinical treatment of cardiovascular diseases such as hypertension. However, the mechanism of how BBR attenuates hypertension through affecting central neural system is not clear.
Purpose: This study was designed to determine whether chronic infusion of BBR into the hypothalamic paraventricular nucleus (PVN) attenuates hypertension and sympathoexcitation via the ROS/Erk1/2/iNOS pathway.
Methods: Two-kidney, one-clip (2K1C) renovascular hypertensive rats were randomly assigned and treated with bilateral PVN infusion of BBR (2μg/h) or vehicle (artificial cerebrospinal fluid) via osmotic minipumps for 28 days.
Results: 2K1C rats showed higher mean arterial pressure (MAP) and PVN Fra-like activity, plasma levels of norepinephrine (NE), PVN levels of NOX2, NOX4, Erk1/2 and iNOS, and lower PVN levels of copper/zinc superoxide dismutase (Cu/Zn-SOD). Chronic infusion of BBR reduced MAP, PVN Fra-like activity and plasma levels of NE, reduced NOX2, NOX4, Erk1/2, iNOS and induced Cu/Zn-SOD in the PVN.
Conclusions: These results suggest that BBR attenuates hypertension and sympathoexcitation via the ROS/Erk1/2/iNOS pathway in 2K1C renovascular hypertensive rats.
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| http://dx.doi.org/10.1016/j.phymed.2018.09.206 | DOI Listing |
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