• Title/Summary/Keyword: RNA virus sensors

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The Innate Immune Viral Sensors and Their Functional Crosstalk

  • Ji-Seung Yoo
    • Microbiology and Biotechnology Letters
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    • v.52 no.2
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    • pp.105-113
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    • 2024
  • The precise and elaborate regulation of signaling cascades by diverse cytoplasmic and endosomal antiviral sensors is crucial for maintaining immune homeostasis and defending against viral pathogens. Receptors and enzymes that recognize foreign nucleic acids play a pivotal role in inducing antiviral interferon programs, serving as the first line of defense against various DNA and RNA viruses. Recent research has increasingly highlighted the crosstalk between nucleic acid sensors in detecting multiple virus invasions, resulting in amplified antiviral signals and compensating for any missing roles. This review provides an update on recent findings regarding the interplay of RNA sensors for DNA virus recognition.

Oxymatrine Causes Hepatotoxicity by Promoting the Phosphorylation of JNK and Induction of Endoplasmic Reticulum Stress Mediated by ROS in LO2 Cells

  • Gu, Li-li;Shen, Zhe-lun;Li, Yang-Lei;Bao, Yi-Qi;Lu, Hong
    • Molecules and Cells
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    • v.41 no.5
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    • pp.401-412
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    • 2018
  • Oxymatrine (OMT) often used in treatment for chronic hepatitis B virus infection in clinic. However, OMT-induced liver injury has been reported. In this study, we aim to investigate the possible mechanism of OMT-induced hepatotoxicity in human normal liver cells (L02). Exposed cells to OMT, the cell viability was decreased and apoptosis rate increased, the intracellular markers of oxidative stress were changed. Simultaneously, OMT altered apoptotic related proteins levels, including Bcl-2, Bax and pro-caspase-8/-9/-3. In addition, OMT enhanced the protein levels of endoplasmic reticulum (ER) stress makers (GRP78/Bip, CHOP, and cleaved-Caspase-4) and phosphorylation of c-Jun N-terminal kinase (p-JNK), as well as the mRNA levels of GRP78/Bip, CHOP, caspase-4, and ER stress sensors (IREI, ATF6, and PERK). Pre-treatment with Z-VAD-fmk, JNK inhibitor SP600125 and N-acetyl-l-cysteine (NAC), a ROS scavenger, partly improved the survival rates and restored OMT-induced cellular damage, and reduced caspase-3 cleavage. SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4. Furthermore, 4-PBA, the ER stress inhibitor, weakened inhibitory effect of OMT on cells, on the contrary, TM worsen. 4-PBA also reduced the levels of p-JNK and cleaved-caspase-3 proteins. Therefore, OMT-induced injury in L02 cells was related to ROS mediated p-JNK and ER stress induction. Antioxidant, by inhibition of p-JNK or ER stress, may be a feasible method to alleviate OMT-induced liver injury.