Han Shuo, Chen Lifu, Zhang Yi, Xie Shihui, Yang Jiali, Su Songkun, Yao Hong, Shi Peiying
Department of Traditional Chinese Medicine Resource and Bee Products, College of Animal Sciences (College of Bee Science), Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Department of Pharmaceutical Analysis, School of Pharmacy, Fujian Medical University, Fuzhou 350122, China.
Antioxidants (Basel). 2022 Dec 30;12(1):88. doi: 10.3390/antiox12010088.
Bee pollen possesses an anti-cardiomyocyte injury effect by reducing oxidative stress levels and inhibiting inflammatory response and apoptosis, but the possible effect mechanism has rarely been reported. This paper explores the effect of the extract of lotus bee pollen (LBPE) on cardiomyocyte hypertrophy (CH) and its mechanism. The main components of LBPE were identified via UPLC-QTOF MS. An isoproterenol-induced rat H9c2 CH model was subsequently used to evaluate the protection of LBPE on cells. LBPE (100, 250 and 500 μg∙mL) reduced the surface area, total protein content and MDA content, and increased SOD activity and GSH content in CH model in a dose-dependent manner. Meanwhile, quantitative real-time PCR trials confirmed that LBPE reduced the gene expression levels of CH markers, pro-inflammatory cytokines and pro-apoptosis factors, and increased the Bcl-2 mRNA expression and Bcl-2/Bax ratio in a dose-dependent manner. Furthermore, target fishing, bioinformatics analysis and molecular docking suggested JAK2 could be a pivotal target protein for the main active ingredients in the LBPE against CH. Ultimately, Western blot (WB) trials confirmed that LBPE can dose-dependently inhibit the phosphorylation of JAK2 and STAT3. The results show that LBPE can protect against ISO-induced CH, possibly via targeting the JAK2/STAT3 pathway, also suggesting that LBPE may be a promising candidate against CH.
蜂花粉通过降低氧化应激水平、抑制炎症反应和细胞凋亡而具有抗心肌细胞损伤作用，但其可能的作用机制鲜有报道。本文探讨莲蜂花粉提取物（LBPE）对心肌细胞肥大（CH）的影响及其机制。通过超高效液相色谱-四极杆飞行时间质谱（UPLC-QTOF MS）鉴定LBPE的主要成分。随后采用异丙肾上腺素诱导的大鼠H9c2心肌细胞肥大模型评估LBPE对细胞的保护作用。LBPE（100、250和500μg∙mL）以剂量依赖性方式降低CH模型中的表面积、总蛋白含量和丙二醛（MDA）含量，并增加超氧化物歧化酶（SOD）活性和谷胱甘肽（GSH）含量。同时，实时定量聚合酶链反应（qRT-PCR）试验证实，LBPE以剂量依赖性方式降低CH标志物、促炎细胞因子和促凋亡因子的基因表达水平，并增加Bcl-2信使核糖核酸（mRNA）表达及Bcl-2/Bax比值。此外，靶点筛选、生物信息学分析和分子对接表明，Janus激酶2（JAK2）可能是LBPE中抗CH主要活性成分的关键靶蛋白。最终，蛋白质免疫印迹法（WB）试验证实，LBPE可剂量依赖性抑制JAK2和信号转导子与转录激活子3（STAT3）的磷酸化。结果表明，LBPE可能通过靶向JAK2/STAT3信号通路对异丙肾上腺素诱导的心肌细胞肥大具有保护作用，这也提示LBPE可能是一种有前景的抗心肌细胞肥大候选物。
