Metformin alleviates chronic obstructive pulmonary disease and cigarette smoke extract-induced glucocorticoid resistance by activating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway

Fulin Tao; Yuanyuan Zhou; Mengwen Wang; Chongyang Wang; Wentao Zhu; Zhili Han; Nianxia Sun; Dianlei Wang

doi:10.4196/kjpp.2022.26.2.95

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자료유형: 학술저널

저자정보: Fulin Tao (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Yuanyuan Zhou (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Mengwen Wang (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Chongyang Wang (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Wentao Zhu (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Zhili Han (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Nianxia Sun (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 China) Dianlei Wang (College of Pharmacy Anhui University of Chinese Medicine Hefei Anhui 230012 ChinaAnhui Province Key)

저널정보: 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제2호

발행연도: 2022.2

수록면: 95 - 111 (17page)

DOI: 10.4196/kjpp.2022.26.2.95

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Chronic obstructive pulmonary disease (COPD) is an important healthcare problem worldwide. Often, glucocorticoid (GC) resistance develops during COPD treatment. As a classic hypoglycemic drug, metformin (MET) can be used as a treatment strategy for COPD due to its anti-inflammatory and antioxidant effects, but its specific mechanism of action is not known. We aimed to clarify the role of MET on COPD and cigarette smoke extract (CSE)-induced GC resistance. Through establishment of a COPD model in rats, we found that MET could improve lung function, reduce pathological injury, as well as reduce the level of inflammation and oxidative stress in COPD, and upregulate expression of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), multidrug resistance protein 1 (MRP1), and histone deacetylase 2 (HDAC2). By establishing a model of GC resistance in human bronchial epithelial cells stimulated by CSE, we found that MET reduced secretion of interleukin- 8, and could upregulate expression of Nrf2, HO-1, MRP1, and HDAC2. MET could also increase the inhibition of MRP1 efflux by MK571 significantly, and increase expression of HDAC2 mRNA and protein. In conclusion, MET may upregulate MRP1 expression by activating the Nrf2/HO-1 signaling pathway, and then regulate expression of HDAC2 protein to reduce GC resistance

#Chronic obstructive pulmonary disease #Glucocorticoid resistance #Metformin #Nuclear factor E2-related factor 2

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