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RISS 인기검색어
- 검색키워드
- 저자 : Ma Yuanqiang (검색결과 3 건)
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Ma Yuanqiang,Jeong su Park,Wang Feng,Hwan Ma,Gyu rim Lee,Yeo jin Lee,Yoon-seok Roh 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Psoriasis, a chronic inflammation-mediated skin disease, affects 2-3% of the total populations in the world. It is characterized by keratinocytes hyperproliferation and immune cell infiltration. The JAK/STAT3 and JAK/STAT1 signaling pathways triggered by IL-6 and IFN- γ from dendritic cell and T lymphocytes, play important roles in psoriasis. Thus, blockade of JAK/STAT signaling will be potential strategy in psoriasis. CMX, an extract of Centipeda minima enriched in Brevilin A, Arnicolide D, Arnicolide C, and Microhelenin C which have already been reported in anti-inflammation, anti-cancer, antiallergy, and suppression of proliferation. We established chronic inflammatory and cell proliferating models in macrophages and keratinocytes with LPS (250ng/mL), rh-IL-6 (10ng/mL), or rh-IFN-γ (10ng/mL) to evaluate the effect of CMX. CCK-8 was used for cell proliferation assay, and the protein and RNA were collected and analyzed by western blot and RT-qPCR. We found that CMX inhibited pro-inflammatory cytokines production by inhibiting LPS-induced JAK1/2 and STAT1/3 phosphorylation in macrophages. Moreover, CMX down-regulated chemokines and cell proliferation in HaCaT cell induced by rh-IL-6 and rh-IFN-γ, respectively. Consistently, we demonstrated that reduction of chemokines expression and hyperproliferation was medicated by the regulation of IFN-γ-activated JAK/STAT1 and IL-6-activated JAK/STAT3 signaling. In conclusion, CMX inhibited JAK/STAT-mediated inflammatory responses and cell proliferation in macrophages and keratinocytes, consequently CMX may improve psoriasis development as an important therapeutic approach.
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Cocaine promotes liver inflammation by mtROS production and loss of mitochondrial membrane potential
Gyurim Lee,Wang Feng,Jeongsu Park,Hwan Ma,Ma Yuanqiang,Yoon-Seok Roh 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Cocaine is a worldwide used drug, but its abuse is associated with physical, psychiatric and social problems. Cocaine abuse has been known to cause liver toxicity, but the mechanism remains unknown. Mitochondrial dysfunction and reactive oxygen species (mtROS) have been suggested to be critical for the progression of drug-induced liver injury and inflammation. Mitochondrial membrane potential(ΔΨm) plays a key role in mitochondrial homeostasis. And loss of mitochondrial membrane potential may reduce cell viability and cause various pathologies. Thus, we investigated cocaine-induced liver injury and inflammation through regulation of mitochondrial quality control. We found that cocaine increases hepatocytes death in dose-dependent manner. Moreover, cocaine increased loss of mitochondrial membrane potential in hepatocytes. Given that damaged mitochondria in hepatocytes increases the production of mtROS and activation of inflammasome in Kupffer cells, we sought to investigate the effect of cocaine on production of mtROS in hepatocytes. Indeed, cocaine increased H₂O₂-induced mtROS in hepatocytes. Interestingly, cocaine increased pro-inflammatory cytokines (TNF-a, IL-1b), chemokines (CCL2, CXCL10) and type Ⅰ Interferons (IFN-a, IFN-b) mRNA expression in Kupffer cells. Furthermore, cocaine induced phospholation of NF-κB and IκB in Kupffer cells. In conclusion, we demonstrated cocaine -mediated mediates liver injury and inflammation by up-regulation of mtROS and loss of mitochondrial membrane potential.
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Feng Wang,JeongSu Park,Hwan Ma,Gyu-rim Lee,Yeojin Lee,Yuanqiang Ma,Yoon-Seok Roh 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
NAFLD is becoming one of the most common chronic liver diseases in the world. One of the features of NAFLD is fat accumulation in the liver, which increased hepatic steatosis, fibrosis, and inflammation. Several different saponins have been identified as the major pharmacologically active ingredients isolated from Panax notoginseng. The most important compounds of saponins are ginsenosides. However, the ginsenoside-specific molecular mechanism of the Saponin has not been known in NAFLD. The mouse NAFLD model was established by feeding with Fast food diet for 16 weeks and treated with Saponin (50 or 150mg / kg) for the last 9 weeks. Saponin extract treatment reversed the FFD-induced elevation in the expression levels of lipogenesis-related genes, including fatty acid synthase (FASN) and MLX-interacting protein-like (MLXIPL), to the levels in NCD-fed mice. Surprisingly, the weight and size of the liver was significantly attenuated in the low- or high-dose saponin extract administered groups, compared with the vehicle group. Saponin contains a significantly increased amount of ginsenosides (Rh1 and Rg2). However, in vitro treatment Rh1 and Rg2 exerted anti-steatosis effect in primary hepatocytes by enhancing mRNA expression of fatty acid oxidation and decreasing lipogenesis related mRNA expression. In addition, saponin extract treatment reduced the FFD-induced collagen deposition according to the Sirius Red staining results as well as significantly decreased the mRNA levels of various fibrosis-related genes in vivo and in vitro. Additionally, ginsenosides Rh1 and Rg2 significantly alleviated the elevated expression of inflammatory genes induced by LPS treatment and FFD administration. Furthermore, ginsenosides Rh1 and Rg2 alleviated NLRP3 inflammasome activation by promoting mitophagy. In conclusion, Saponin inhibited the activation of inflammasome in macrophages, which in turn prevents NAFLD development. Thus, the administration of Saponin might be an alternative for the prevention of NAFLD.
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