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RUICHEN ZHANG,NENG LIU 서울대학교 사회발전연구소 2020 Journal of Asian Sociology Vol.49 No.1
Existing literature on China’s system of petitioning (xinfang) usually takes a perspective of institutional change or social problematization, understanding it as either a malfunctioning institution or an indicator of governance crises. This article utilizes a normalization perspective instead, seeing xinfang as an understandable, even rational practice of specific individuals. Based on participant observations in Dongzhuang, Beijing, and in-depth interviews with petitioners in the neighborhood, this article aims to reveal the social mechanisms involved in the so-called normalized xinfang, suggesting that structure and agency are weaved together in this process of reproducing motives and perceived realities, which then leads to the continuation of xinfang practice. The article contributes to a more comprehensive understanding of how individual petitioners persevere through multiple crises in their encounters with structural socio-political realities via meaning making and self-construction. Our study helps uncover the somehow neglected micro foundation of the macro level dilemma of enduring xinfang in China.
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Prevention of acetaminophen-induced hepatocyte injury: JNK inhibition and GSTA1 involvement
Chang Yicong,He Jingshan,Ma Bingke,Ishfaq Muhammad,Wang Jiaqi,Zhang Ruichen,Yuan Liang,Liu Jiarui,Li Changwen,Liu Fangping 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.2
Background Glutathione S-transferase A1 (GSTA1) is a detoxification enzyme and a sensitive marker for hepatotoxicity. We investigated the effects of JNK inhibition on different degrees of Acetaminophen (APAP)-induced hepatocyte injury and GSTA1 expression. Objective This study aimed to investigate the role of JNK signaling pathway in APAP-induced different degrees of hepatocyte injury and its correlation with GSTA1 by inhibiting the phosphorylation of JNK by SP600125. Results 6 and 8 mM APAP induced different degrees of hepatocyte injury and apoptosis, both activated JNK signaling pathway. In contrast, JNK inhibitor significantly reduced activation of JNK and c-JUN on exposure to APAP. Meanwhile, the levels of hepatocyte injury, oxidative stress, and apoptosis obviously decreased. Importantly, GSTA1 expression was significantly increased by JNK inhibition. Conclusions JNK inhibition attenuates APAP-induced hepatocyte injury and oxidative stress and increases GSTA1 expression. Furthermore, GSTA1 may be involved in this signaling pathway for detoxification. Background Glutathione S-transferase A1 (GSTA1) is a detoxification enzyme and a sensitive marker for hepatotoxicity. We investigated the effects of JNK inhibition on different degrees of Acetaminophen (APAP)-induced hepatocyte injury and GSTA1 expression. Objective This study aimed to investigate the role of JNK signaling pathway in APAP-induced different degrees of hepatocyte injury and its correlation with GSTA1 by inhibiting the phosphorylation of JNK by SP600125. Results 6 and 8 mM APAP induced different degrees of hepatocyte injury and apoptosis, both activated JNK signaling pathway. In contrast, JNK inhibitor significantly reduced activation of JNK and c-JUN on exposure to APAP. Meanwhile, the levels of hepatocyte injury, oxidative stress, and apoptosis obviously decreased. Importantly, GSTA1 expression was significantly increased by JNK inhibition. Conclusions JNK inhibition attenuates APAP-induced hepatocyte injury and oxidative stress and increases GSTA1 expression. Furthermore, GSTA1 may be involved in this signaling pathway for detoxification.
KCI
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