http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Dianlei Wang (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Fulin Tao,Yuanyuan Zhou,Mengwen Wang,Chongyang Wang,Wentao Zhu,Zhili Han,Nianxia Sun,Dianlei Wang 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.2
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
-
Jie Wu,Xueqi Wang,Zhaomin Yao,Qingqing Wu,Wei Fang,Zegeng Li,Dianlei Wang 대한약학회 2019 Archives of Pharmacal Research Vol.42 No.11
In the present study, the roles of AITC in upregulatingthe MRP1 expression and its relationship with theactivation of the Notch1 signaling pathway were investigatedby combining the in vivo and in vitro experiments. AITCwas administered to the COPD model rats and normal ratsto explore the association between Notch1 and MRP1. Thehuman bronchial epithelial cells were treated with DAPT,the Notch1 signaling pathway inhibitor, to verify the effectof Notch1 on the expression of AITC-induced MRP1. Comparedwith the control group, the expressions of Notch1,Hes1 (the target gene of Notch1) and MRP1 in the lung tissueof the COPD model group were significantly inhibited. In contrast to the COPD model group, the expressions ofMRP1, Hes1 and Notch1 dramatically up-regulated followingthe treatment with Low/High doses of AITC. The expressionof MRP1 in the 16 HBE cells was down-regulated bythe inhibition of Notch in a DAPT concentration-dependentmanner. Additionally, the AITC-induced up-regulation ofthe MRP1 expression was markedly impaired following the inhibition of Notch1. The above results indicated that thepulmonary function and the expression of MRP1 in COPDrats could be improved by AITC, which was partly dependenton the Notch1 signaling pathway. Therefore, targetingthe Notch signaling pathway may present as an effectivetherapeutic strategy for COPD treatment.
-
Lingling Xu,Jie Wu,Nini Li,Chengjun Jiang,Yan Guo,Peng Cao,Dianlei Wang 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.6
The present study aimed to examine the effect of allyl isothiocyanate (AITC) on chronic obstructive pulmonary disease and to investigate whether upregulation of multidrug resistance-associated protein 1 (MRP1) associated with the activation of the PARK7 (DJ-1)/nuclear factor erythroid 2-related factor 2 (Nrf2) axis. Lung function indexes and histopathological changes in mice were assessed by lung function detection and H&E staining. The expression levels of Nrf2, MRP1, heme oxygenase-1 (HO-1), and DJ-1 were determined by immunohistochemistry, Western blotting and reverse transcription-quantitative polymerase chain reaction. Next, the expression of DJ-1 in human bronchial epithelial (16HBE) cells was silenced by siRNA, and the effect of DJ-1 expression level on cigarette smoke extract (CSE)-stimulated protein degradation and AITC-induced protein expression was examined. The expression of DJ-1, Nrf2, HO-1, and MRP1 was significantly decreased in the wild type model group, while the expression of each protein was significantly increased after administration of AITC. Silencing the expression of DJ-1 in 16HBE cells accelerated CSE-induced protein degradation, and significantly attenuated the AITC-induced mRNA and protein expression of Nrf2 and MRP1. The present study describes a novel mechanism by which AITC induces MRP1 expression by protecting against CS/CSEmediated DJ-1 protein degradation via activation of the DJ-1/Nrf2 axis.
ScienceON
스콜라연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
