Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158
  • Jie Xu, Shouzhu Xu, Jiayin Luo, Shihao Zhang, Dongdong Wu, Qifan Yang, ...
    論文ID: b23-00773
    発行日: 2024年
    [早期公開] 公開日: 2024/06/12
    ジャーナル フリー 早期公開

    Ethanol (alcohol) is a risk factor that contributes to non-communicable diseases. Chronic abuse of ethanol is toxic to both the heart and overall health, and even results in death. Ethanol and its byproduct acetaldehyde can harm the cardiovascular system by impairing mitochondrial function, causing oxidative damage, and reducing contractile proteins. Endothelial cells are essential components of the cardiovascular system, are highly susceptible to ethanol, either through direct or indirect exposure. Thus, protection against endothelial injury is of great importance for persons who chronic abuse of ethanol. In this study, an in vitro model of endothelial injury was created using ethanol. The findings revealed that a concentration of 20.0 mM of ethanol reduced cell viability and Bcl-2 expression, while increasing cell apoptosis, intracellular ROS levels, mitochondrial depolarization, and the expression of Bax and cleaved-caspase-3 in endothelial cells. Further study showed that ethanol promoted nuclear translocation of NF-κB, increased the secretion of TNF-α,IL-1β, IL-6 in the culture medium, and inhibited Nrf2 signaling pathway. The aforementioned findings suggest that ethanol has a harmful impact on endothelial cells. Nevertheless, the application of epigallocatechin-3-gallate (EGCG) to the cells can effectively mitigate the detrimental effects of ethanol on endothelial cells. In conclusion, EGCG alleviates ethanol-induced endothelial injury partly through alteration of NF-κB translocation and activation of the Nrf2 signaling pathway. Therefore, EGCG holds great potential in safeguarding individuals who chronically abuse ethanol from endothelial dysfunction.

  • Xin Wang, Qing Liu
    論文ID: b21-00329
    発行日: 2021年
    [早期公開] 公開日: 2021/08/20
    ジャーナル フリー 早期公開

    Neuropathic pain is one of the most intractable diseases. The lack of effective therapy measures remains a critical problem due to the poor understanding of the cause of neuropathic pain. The aim of this study was to investigate the effect of dexmedetomidine (Dex) in trigeminal neuropathic pain and the underlying molecular mechanism in order to identify possible therapeutic targets. We used a chronic constriction injury (CCI) model of mice to investigate whether Dex prevents neuropathic pain and the inflammation response. The α 2-adrenoceptors (α2AR) inhibitor BRL44408 and adenovirus for knocking down High mobility group box 1 (HMGB1) was administrated to confirm whether Dex exert its effect through targeting α2AR and HMGB1. The results indicated that Dex significantly inhibited CCI induced neuropathic pain through targeting α2AR and HMGB1. Dex inhibited the inflammatory response through decreasing the release and the mRNA expression of IL-1β, IL-6, and TNF-ɑ while increasing that of IL-10. Moreover, Dex participates in the regulation of HMGB1, Toll-like receptor 4 (TLR4), NFκb (p-65) expression and the phosphorylation of IκB-ɑ. In conclusion, Dex could relieve neuropathic pain through α2AR and HMGB1 and attenuate inflammation response.