Medicinal Foods, YT and RH Combination, Suppress Cigarette Smoke-Induced Inflammation and Oxidative Stress by Inhibiting NF-κB/ERK Signaling Pathways

Abstract

Background. Cigarette smoke is a risk factor for Chronic Obstructive Pulmonary Disease (COPD). Given the lack of COPD curative treatment, dietary management for COPD patients has become important. This study investigated whether the medicinal foods (YT and RH) could suppress cigarette smoke exposure-induced inflammation and oxidative stress. Methods. Chronic pulmonary inflammation in male C57 mice was induced by a 4-week exposure to cigarette smoke (CS). The medicinal foods YT and RH were orally administered 1 week prior to CS exposure. The protective effects were assessed by measuring the pulmonary function and histopathological evaluations. Inflammatory cell numbers and cytokines levels in BALF and blood serum were analyzed by enzyme-linked immunosorbent assay (ELISA). Malondialdehyde (MDA) and superoxide dismutase (SOD) levels of the lung were analyzed. Furthermore, the levels of phosphorylated ERK and NF-κB in both the mice lungs and RAW264.7 cells were also detected. Results. YT and RH combination (YT + RH) significantly improved pulmonary function and suppressed the inflammation, including cell number and cytokines in BALF relative to the CS group; histological examination revealed protective effects of YT + RH in the lungs of mice exposed to CS. Moreover, the MDA level in the lung of the YT + RH group of mice was lower, the SOD activity was higher, and in vitro treatment of YT and RH combination attenuated reactive oxygen species (ROS) expression in mouse macrophage RAW264.7 cells stimulated with cigarette smoke (CSE). YT + RH combination significantly reduced the expression of pNF-κB and pERK in the lung tissues and macrophage stimulated with CSE. Conclusions. YT and RH combination attenuates cigarette smoke-induced inflammation and oxidative stress through inhibition of the NF-κB/ERK signaling pathway.

Evaluation of the Effects of e-Cigarette Aerosol Extracts and Tobacco Cigarette Smoke Extracts on RAW264.7 Cells

“…Oxidative stress occurs when ROS production exceeds the antioxidant capacity, resulting in damage to cellular components such as DNA, lipids, and proteins. This damage can lead to cell death and extracellular matrix degradation. , Moreover, cellular oxidative stress triggers a cascade of inflammatory responses in humans . CS is known to induce substantial ROS production, mainly released by activated cells, including macrophages, neutrophils, and structural cells. , Excessive ROS accumulation can also induce cell senescence, which is a significant risk factor for conditions like hypertension and chronic obstructive pulmonary disease (COPD) .…”

“… 36 , 37 Moreover, cellular oxidative stress triggers a cascade of inflammatory responses in humans. 38 CS is known to induce substantial ROS production, mainly released by activated cells, including macrophages, neutrophils, and structural cells. 39 , 40 Excessive ROS accumulation can also induce cell senescence, which is a significant risk factor for conditions like hypertension and chronic obstructive pulmonary disease (COPD).…”