Abstract Context Baicalin is an active compound which demonstrates cardioprotection effects against myocardial ischaemia/reperfusion injury (MI/RI). Objective To investigate how baicalin protects against myocardial injury and to explore its potential mechanism. We hypothesized that baicalin-modulated macrophages change from M1 (pro-inflammatory subset) to M2 (anti-inflammatory subset) under I/R stress. Materials and methods We established an ischaemia/reperfusion (I/R) model using Sprague Dawley (SD) rat, then baicalin was intragastric administration (20, 60 or 120 mg/kg) for 24 h. The rats were randomly divided into five groups (n = 10): control, I/R, I/R + baicalin (20 mg/kg), I/R + baicalin (60 mg/kg) and I/R + baicalin (120 mg/kg). Cardiac function was detected by echocardiography, HE staining and ELISA, respectively. Macrophage phenotype was examined by flow cytometry. Furthermore, IHC, qRT-PCR and WB were employed to analyse the related mechanisms. Results The study showed that baicalin (20, 60 or 120 mg/kg) significantly improved cardiac function and impeded cardiac apoptosis in rats. In addition, the repair of myocardial morphology (reduced neutrophil infiltration) further confirmed its cardiacprotective effect. Moreover, baicalin effectively decreased iNOS, IL-1β and IL-6, and up-regulated Arg-1, IL-10 and TGF-β via changing the macrophage phenotype (from M1 towards M2). Notably, treatment with baicalin also inhibited the phosphorylation levels of JAK2 and STAT3. Discussion and conclusions: It was confirmed that baicalin alleviated post-I/R myocardial injury and reduced inflammation via JAK/STAT pathway, and baicalin treatment might be recommended as a new approach for myocardial ischaemic complications.

中文翻译：

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黄芩苷通过抑制JAK/STAT通路调节巨噬细胞极化减轻心肌缺血/再灌注损伤

摘要背景黄芩苷是一种活性化合物，对心肌缺血/再灌注损伤（MI/RI）具有心脏保护作用。目的探讨黄芩苷对心肌损伤的保护作用，并探讨其可能的机制。我们假设黄芩素调节的巨噬细胞在 I/R 应激下从 M1（促炎子集）变为 M2（抗炎子集）。材料与方法 我们使用 Sprague Dawley (SD) 大鼠建立缺血/再灌注 (I/R) 模型，然后黄芩苷灌胃 (20、60 或 120 mg/kg) 24 h。将大鼠随机分为5组（n=10）：对照、I/R、I/R+黄芩苷（20mg/kg）、I/R+黄芩苷（60mg/kg）和I/R+黄芩苷（ 120 毫克/公斤）。分别通过超声心动图、HE染色和ELISA检测心脏功能。通过流式细胞术检查巨噬细胞表型。此外，采用 IHC、qRT-PCR 和 WB 来分析相关机制。结果 研究表明，黄芩苷（20、60 或 120 mg/kg）可显着改善大鼠的心功能并阻止心脏细胞凋亡。此外，心肌形态的修复（中性粒细胞浸润减少）进一步证实了其心脏保护作用。此外，黄芩苷通过改变巨噬细胞表型（从 M1 到 M2）有效降低 iNOS、IL-1β 和 IL-6，并上调 Arg-1、IL-10 和 TGF-β。值得注意的是，黄芩苷处理也抑制了 JAK2 和 STAT3 的磷酸化水平。讨论与结论：证实黄芩苷通过JAK/STAT通路减轻I/R后心肌损伤并减轻炎症，