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Protective Effects of Different Kinds of Filtered Water on Hypertensive Mouse by Suppressing Oxidative Stress and Inflammation


Hydrogen Water Studies

High Blood PressureCardiac Hypertrophy

Protective Effects of Different Kinds of Filtered Water on Hypertensive Mouse by Suppressing Oxidative Stress and Inflammation

by Chan Lu, Fan Xin, Guohong Ruan, Qian Sun, Ronghe Chen, Xinan Wen

Abstract:

Oxidative stress and inflammation play an important role in hypertensive animals and patients. Hydrogen plays a role of antioxidation and anti-inflammation. Calcium and magnesium play an important role in reducing hypertension and antioxidant. Filtered water contains abundant hydrogen and a large number of other essential elements of the human body. We investigated the protective effects of filtered water on hypertensive mice. To establish hypertension model, ICR mice were administered with N-nitro-L-arginine methyl ester (L-NAME) hydrochloride 64 mg/kg per day for 1 month. The hypertensive mice were, respectively, administered with pure water, tap water, and filtered water for 2 months. Lipid peroxidation, antioxidant enzymatic activity, endothelin-1 (ET-1), angiotensin II (Ang II), and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) were assessed. Expressions of phosphorylated NF-κB P65 in the kidney were analyzed by western blot. qRT-PCR analysis was adopted to determine the expression levels of the pro-inflammatory cytokines and NF-κB P65. The results demonstrated that filtered water can reduce the blood pressure. Filtered water treatment restored the activity of antioxidant enzymes, downregulated ET-1, and Ang II in the serum of mice. Filtered water treatment suppressed pro-inflammatory cytokines and decreased the mRNA expression of TNF-α, IL-6, IL-1β, and NF-κB P65. Consumption of filtered water inhibited the expression of NF-κB P65. This suggests that filtered water can reduce the blood pressure. The protection mechanisms include downregulating oxidative stress and inhibiting inflammation, which is partly due to the inhibition of the NF-κB signaling pathway.

Read more:

https://doi.org/10.1155/2018/2917387

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Sam Soliman

Research Scientist at iBottle

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