The therapeutic potential of quercetin for cigarette smoking–induced chronic obstructive pulmonary disease: a narrative review

Abstract

Quercetin is a flavonoid with antioxidant and anti-inflammatory properties. Quercetin has potentially beneficial therapeutic effects for several diseases, including cigarette smoking–induced chronic obstructive pulmonary disease (CS-COPD). Many studies have shown that quercetin’s antioxidant and anti-inflammatory properties have positive therapeutic potential for CS-COPD. In addition, quercetin’s immunomodulatory, anti-cellular senescence, mitochondrial autophagy–modulating, and gut microbiota–modulating effects may also have therapeutic value for CS-COPD. However, there appears to be no review of the possible mechanisms of quercetin for treating CS-COPD. Moreover, the combination of quercetin with common therapeutic drugs for CS-COPD needs further refinement. Therefore, in this article, after introducing the definition and metabolism of quercetin, and its safety, we comprehensively presented the pathogenesis of CS-COPD related to oxidative stress, inflammation, immunity, cellular senescence, mitochondrial autophagy, and gut microbiota. We then reviewed quercetin’s anti-CS-COPD effects, performed by influencing these mechanisms. Finally, we explored the possibility of using quercetin with commonly used drugs for treating CS-COPD, providing a basis for future screening of excellent drug combinations for treating CS-COPD. This review has provided meaningful information on quercetin’s mechanisms and clinical use in treating CS-COPD.

Amelioration of Oxidative Stress in Rats with Chronic Obstructive Pulmonary Disease through Shenqi Huatan Decoction Activation of Peroxisome Proliferator‐Activated Receptor Gamma‐Mediated Activated Protein Kinase/Forkhead Transcription Factor O3a Signaling Pathway

“…The primary sources of exogenous ROS are cigarette smoke and airborne particulate matter [ 8 ]. High levels of free radicals and other oxidants in cigarette smoke dissolve in the fluid that lines the airway epithelium upon entry into the airways, accumulate in the lungs, irritate the lung tissue over time, sustain inflammation, and aid in developing COPD [ 9 ]. The inflammatory response and hypoxia are essential factors in producing endogenous ROS.…”

Association of Dietary Flavonoid Intake with Serum Cotinine Levels in the General Adult Population

“…Smoking has been identified as a primary cause of numerous diseases, including cardiovascular diseases, COPD, diabetes, and cancer. The highly reactive nature of the free radicals generated by nicotine can lead to cellular and subcellular structural damage, affecting proteins, nucleic acids, and lipids [33]. Excessive oxidative damage can trigger severe inflammatory reactions, resulting in ROS accumulation [34].…”

“…Concerning total flavonoids, a negative linear association was observed when intake remained below 99.61 mg/day. (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)40-59, or ≥60), sex (male or female), and race/ethnicity (Mexican American, Other Hispanic, Non-Hispanic White, Non-Hispanic Black, or Other), education level (below high school, high school, or above high school), family poverty income ratio (≤1.0, 1.1-3.0, or >3.0), drinking status (nondrinker, low-to-moderate drinker, or heavy drinker), energy intake levels (in quartiles), BMI (<25.0, 25.0-29.9, or >29.9), and supplement use (yes or no); Model 2 was adjusted as model 1 plus smoking status (never smoker, former smoker, or current smoker).…”

“…The dietary flavonoid intake with the largest weight in the serum cotinine levels was anthocyanidins (32.30%), followed by Isoflavones (26.80%), flavones (19.50%), flavanones (18.80%), and flavan-3-ols (2.49%), and the detailed weight of each dietary flavonoid intake is presented in Figure 2. (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59), or ≥60), sex (male or female), and race/ethnicity (Mexican American, Other Hispanic, Non-Hispanic White, Non-Hispanic Black, or Other), education level (below high school, high school, or above high school), family PIR (≤1.0, 1.1-3.0, or >3.0), drinking status (nondrinker, low-to-moderate drinker, or heavy drinker), energy intake levels (in quartiles), BMI (<25.0, 25.0-29.9, or >29.9), supplement use (yes or no), and smoking status (never smoker, former smoker, or current smoker).…”

Nicotine: From Discovery to Biological Effects

“…Several natural compounds have been analyzed for their ability to counteract the effects induced by nicotine [93][94][95]. The following compounds appear to be of potential interest:…”