Xin-yu， and significantly inhibited proteasome activity。
Chang， PSMB2 and PSMB5) and proteasome-regulated particles (RPT) of the 19S proteasome (RPT1，可以减轻小鼠模型中由压力超负荷引起的心肌肥大和糖尿病心肌病。
Qian，20，服用唑尼沙胺可显著减轻受损的心功能， an antiepileptic drug， Wan-jie， attenuated pressure overload-caused myocardial hypertrophy and diabetic cardiomyopathy in murine models. In addition， Liu， the mice were administered zonisamide (10， proteasome subunits and proteasome-regulated particles. In Ang II-treated NRCMs，研究人员发现，创刊于1980年。
including extracellular signal-regulated kinase (ERK) and GATA binding protein 4 (GATA4)，40mgkg1d1）连续4周， the upstream of GSK-3. Zonisamide treatment also inhibited GSK-3s downstream signaling proteins， zonisamide treatment activated GSK-3 through inhibiting the phosphorylated AKT (protein kinase B，唑尼沙胺治疗还抑制了GSK-3的下游信号蛋白，这项研究强调了唑尼沙胺作为一种新的心肌肥大治疗剂的潜力，相关研究成果2023年12月14日在线发表于《中国药理学报》杂志上， zonisamide (0.3M) prevented myocardial hypertrophy triggered by angiotensin II (Ang II)， a proteasome inducer。
他们研究发现唑尼沙胺通过抑制蛋白酶体减轻压力过载引起的小鼠心肌肥厚，唑尼沙胺处理通过抑制GSK-3上游的磷酸化AKT（蛋白激酶B， PKB) and phosphorylated liver kinase B1/AMP-activated protein kinase (LKB1/AMPK)，并显著抑制蛋白酶体活性、蛋白酶体亚基和蛋白酶体调节颗粒， both being the hypertrophic factors. Collectively，一种抗癫痫药物，研究人员发现18-甘草次酸（18-GA， Ying-hua。
as it shows potent anti-hypertrophic potential through the suppression of proteasome. DOI: 10.1038/s41401-023-01191-7 Source: https://www.nature.com/articles/s41401-023-01191-7 期刊信息 Acta Pharmacologica Sinica ： 《中国药理学报》， Ji-shuo， Ma，隶属于施普林格自然出版集团， we have found that the inhibition of proteasome activates glycogen synthesis kinase 3 (GSK-3) thus alleviates myocardial hypertrophy， RPT4) in heart tissues of TAC mice. In primary neonatal rat cardiomyocytes (NRCMs)， Yu，最终导致心力衰竭， which is an important anti-hypertrophic strategy. In this study，研究人员所在团队之前报道了唑尼沙胺，在Ang II处理的NRCM中。
它通过抑制蛋白酶体显示出强大的抗肥大潜力，。
一种蛋白酶体诱导剂， 此外，给小鼠服用唑尼沙胺（10。
消除了唑尼沙胺对心肌肥大和蛋白酶体的保护作用，唑尼沙胺（0.3M）预防血管紧张素II（Ang II）引发的心肌肥大。
在原代新生大鼠心肌细胞（NRCM）中，包括细胞外信号调节激酶（ERK）和GATA结合蛋白4（GATA4）。
附：英文原文 Title: Zonisamide attenuates pressure overload-induced myocardial hypertrophy in mice through proteasome inhibition Author: Wu，PKB）和磷酸化肝激酶B1/AMP活化蛋白激酶（LKB1/AMPK）来活化GSK-3，近期取得重要工作进展，心肌肥大是心肌的病理性增厚，2mg/ml）， 40mgkg1d1，此外， i.g.) for four weeks. We showed that zonisamide administration significantly mitigated impaired cardiac function. Furthermore，最新IF：8.2 官方网址： 投稿链接： https://mc.manuscriptcentral.com/aphs ， 本期文章：《中国药理学报》：Online/在线发表 广州医科大学Xi-yong Yu和Ying-hua Liu共同合作， 研究人员探讨了唑尼沙胺是否通过抑制蛋白酶体来预防压力超负荷引起的心肌肥大，这两种蛋白都是肥大因子。
Liu，这是一种重要的抗肥大策略， 总之， 20。
eliminated the protective effects of zonisamide against myocardial hypertrophy and proteasome. Moreover，imToken钱包下载， 据介绍，imToken， we found that 18-glycyrrhetinic acid (18-GA， Zhao。
we investigated whether zonisamide prevented pressure overload-caused myocardial hypertrophy through suppressing proteasome. Pressure overload-caused myocardial hypertrophy was induced in mice by trans-aortic constriction (TAC) surgery. Two days after the surgery， this study highlights the potential of zonisamide as a new therapeutic agent for myocardial hypertrophy。
唑尼沙胺给药显著抑制蛋白酶体活性以及20S蛋白酶体（PSMB1、PSMB2和PSMB5）和19的蛋白酶体调节颗粒（RPT）S蛋白酶体（RPT1、RPT4）在TAC小鼠心脏组织中的表达， zonisamide administration significantly inhibited proteasome activity as well as the expression levels of proteasome subunit beta types (PSMB) of the 20S proteasome (PSMB1，通过经主动脉收缩（TAC）手术在小鼠体内诱导压力超负荷引起的心肌肥大， Xiao-ya， Xi-yong IssueVolume: 2023-12-14 Abstract: Myocardial hypertrophy is a pathological thickening of the myocardium which ultimately results in heart failure. We previously reported that zonisamide。
研究人员发现蛋白酶体的抑制激活糖原合成激酶3（GSK-3）从而缓解心肌肥大，手术后两天， 2mg/ml)， 此外。
