Rice Bran Oil Improves Emphysema in Cigarette Smoke Extract-Induced Mice through Anti-Inflammatory and Antioxidative Effects

Kettawan, Aikkarach; Ruangklai, Sukpattaraporn; Rungruang, Thanaporn; Thongam, Julalux; Kettawan, Aurawan Kringkasemsee; Nirmal, Nilesh; Srisuma, Sorachai

doi:10.3390/nu16030433

Cited by 3 publications

(1 citation statement)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The IP injection model can also be established without the requirement of a longer treatment time (usually 3-6 weeks) [38,39]. Recent studies comparing CS exposure with IP injection models demonstrated comparable preclinical outcomes when looking at key COPD features, including the extent of lung damages (emphysema) and lung inflammatory changes [19,[40][41][42]. Nonetheless, mice exposed to CSE represent one of the most commonly used models of COPD [34,35,39].…”

Section: Discussionmentioning

confidence: 99%

NADH Intraperitoneal Injection Prevents Lung Inflammation in a BALB/C Mice Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

Slama,

Abdellatif,

Bahria

et al. 2024

Cells

View full text Add to dashboard Cite

Cigarette smoke is one of the main factors in Chronic Obstructive Pulmonary Disease (COPD), a respiratory syndrome marked by persistent respiratory symptoms and increasing airway obstruction. Perturbed NAD+/NADH levels may play a role in various diseases, including lung disorders like COPD. In our study, we investigated the preventive effect of NADH supplementation in an experimental model of COPD induced by cigarette smoke extract (CSE). N = 64 mice randomly distributed in eight groups were injected with NADH (two doses of 100 mg/kg or 200 mg/kg) or dexamethasone (2 mg/kg) before being exposed to CSE for up to 9 weeks. Additionally, NADH supplementation preserved lung antioxidant defenses by preventing the functional loss of key enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase, and the expression levels of glutathione (GSH) (n = 4, p < 0.001). It also reduced oxidative damage markers, such as malondialdehyde (MDA) and nitrites (n = 4, p < 0.001). A marked increase in tissue myeloperoxidase activity was assessed (MPO), confirming neutrophils implication in the inflammatory process. The latter was significantly ameliorated in the NADH-treated groups (p < 0.001). Finally, NADH prevented the CSE-induced secretion of cytokines such as Tumor Necrosis Factor alpha (TNF-α), IL-17, and IFN-y (n = 4, p < 0.001). Our study shows, for the first time, the clinical potential of NADH supplementation in preventing key features of COPD via its unique anti-inflammatory and antioxidant properties.

show abstract

Section: Discussionmentioning

confidence: 99%

NADH Intraperitoneal Injection Prevents Lung Inflammation in a BALB/C Mice Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

Slama,

Abdellatif,

Bahria

et al. 2024

Cells

View full text Add to dashboard Cite

show abstract

Bexarotene ameliorated the pulmonary inflammation and M1 polarization of alveolar macrophages induced by cigarette smoke via PPARγ/HO-1

Feng,

Li,

Zheng

2024

Respir Res

View full text Add to dashboard Cite

Background Alveolar macrophages (AMs) modulate pulmonary inflammation in chronic obstructive pulmonary disease (COPD), contributing to its progression. The PPARγ/RXRα heterodimer influences AM polarization induced by cigarette smoke (CS). Although PPARγ agonists suppress CS-induced M1 macrophage polarization, the impact of RXRα agonists on this process has not been determined. This study explored the effects and mechanisms of the RXRα agonist bexarotene on macrophage polarization in a COPD mouse model. Methods C57BL/6 mice were assigned to the control, model, bexarotene, or model + bexarotene group. The COPD model was induced by CS exposure and intraperitoneal injection of cigarette smoke extract (CSE), followed by intraperitoneal administration of bexarotene. Additionally, MH-S cells were exposed to CSE and bexarotene. Lung tissues were subjected to hematoxylin-eosin staining, and emphysema and inflammatory scores were assessed. Cytokine levels and cell differentials in bronchoalveolar lavage fluid were measured, and macrophage polarization was evaluated using immunohistochemistry, flow cytometry, and qPCR. Results Bexarotene effectively reduced inflammatory scores, cytokine levels, and neutrophil counts and ameliorated emphysema and M1 polarization of AMs in COPD model mice. Furthermore, while CSE exposure reduced PPARγ expression and the transcriptional activity of AMs, bexarotene enhanced the transcriptional response of PPARγ to CSE. HO-1 was identified as a potential target of PPARγ; its levels were assessed in AMs, revealing that bexarotene mitigated the CSE-induced reduction in HO-1. Notably, the effect of bexarotene was partially inhibited by the PPARγ inhibitor. Conclusions Our results indicated that bexarotene may curb inflammation and M1 polarization in COPD through activation of the PPARγ/HO-1 pathway. Supplementary Information The online version contains supplementary material available at 10.1186/s12931-024-03064-x.

show abstract

Research Progress on the Mechanism of Chronic Obstructive Pulmonary Disease Complicated with Osteoporosis

杨

2024

ACM

View full text Add to dashboard Cite

Rice Bran Oil Improves Emphysema in Cigarette Smoke Extract-Induced Mice through Anti-Inflammatory and Antioxidative Effects

Cited by 3 publications

References 57 publications

NADH Intraperitoneal Injection Prevents Lung Inflammation in a BALB/C Mice Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

NADH Intraperitoneal Injection Prevents Lung Inflammation in a BALB/C Mice Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

Bexarotene ameliorated the pulmonary inflammation and M1 polarization of alveolar macrophages induced by cigarette smoke via PPARγ/HO-1

Research Progress on the Mechanism of Chronic Obstructive Pulmonary Disease Complicated with Osteoporosis

Contact Info

Product

Resources

About