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- 저자 : Tang Junxia (검색결과 2 건)
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Yue Yifeng,Zong Liwu,Chen Yongmin,Nianhai Feng,Tang Junxia,Xu Hongyu,Zhao Meiling 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4
Background Inflammation and oxidative stress-induced molecular death are one of the important causes for lung injury in critically ill patients. LKB1 is an important protein kinase in the body and has regulated inflammation and oxidative stress. However, LKB1 control inflammation and oxidative stress in lung injury were unclear. Objective We aimed to investigate the function and mechanism of Liver kinase B1 (LKB1) in lipopolysaccharide (LPS)-induced lung injury. Result LKB1 prevented lung injury, and weakened correlation oxidative stress and inflammatory reaction in LPS-induced mice model of lung injury. Up-regulation of LKB1 reduced reactive oxygen species (ROS) production and it-induced oxidative stress, and weakened inflammatory reactions in LPS-induced lung injury A549 cells. Down-regulation of LKB1 increased ROS production and it-induced oxidative stress, and enhanced inflammatory reactions in LPS-induced lung injury A549 cells. LKB1 induced phosphorylation (p)-AMPK protein expression, and suppressed the protein expression of NLRP3 in LPS-induced mice model of lung injury and in LPS-induced lung injury A549 cells. This experiment demonstrated the inhibition of AMPK or activation of NLRP3 inflammasome reversed the anti-inflammation function of LKB1 in LPS-induced lung injury. Meanwhile, ROS-induced oxidative stress also participated in the anti-inflammation effects of LKB1 in LPS-induced lung injury. Conclusion Therefore, our results indicate that LKB1 reduced inflammation and oxidative stress by regulating the AMPK/NLRP3 signaling pathway in LPS-induced lung injury.
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Melatonin Attenuates Mitochondrial Damage in Aristolochic Acid-Induced Acute Kidney Injury
Sun Jian,Pan Jinjin,Liu Qinlong,Cheng Jizhong,Tang Qing,Ji Yuke,Cheng Ke,wang Rui,Liu Liang,Wang Dingyou,Wu Na,Zheng Xu,Li Junxia,Zhang Xueyan,Zhu Zhilong,Ding Yanchun,Zheng Feng,Li Jia,Zhang Ying,Yua 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.1
Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN). AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.
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