Department of Nutrition, University of Nevada, Reno, Reno, NV 89557, USA.
Environmental Sciences Program, University of Nevada, Reno, Reno, NV 89557, USA.
Biomolecules. 2023 Aug 22;13(9):1274. doi: 10.3390/biom13091274.
Evidence suggests that food bioactives affect the epigenome to prevent pathological cardiac hypertrophy. Recently, we showed that emodin, an anthraquinone, attenuated pathological cardiac hypertrophy and histone deacetylase (HDAC) activity. However, we only examined the cardioprotective effects of emodin's parent compound and not those of emodin metabolites or of emodin-gut microbiome interactions. The microbiome has emerged as a key player in chronic diseases such as metabolic and cardiac disease. Thus, we hypothesized that emodin could reverse hypertension-induced changes in microbial communities.
Normo- and hypertensive (angiotensin II) C57/BL6 female mice were randomly assigned to receive a vehicle (Veh; DMSO:PEG 1:1) or emodin (Emod; 30 mg/kg) for 14 days. Body weights were collected pre- and post-treatment, and blood pressure was assessed via tail cuff. At the study's end, the mice were euthanized and assessed for their heart weights. In addition, stool samples and cecal contents were collected to elucidate changes in the microbial populations using 16S rRNA sequencing. Lastly, the tissue was lysed, and RNA was isolated for qPCR. One-way ANOVA with Tukey's post hoc test was performed unless otherwise specified, and < 0.05 was considered significant.
Emodin significantly attenuated cardiac hypertrophy in the female mice. No significant changes were observed in body weight or systolic blood pressure in response to hypertension or emodin. Lastly, analysis suggests that hypertension altered the microbiome in the cecum and cecal content, with additional evidence to support that emodin affects gut microbiota in the feces and colon.
Our data demonstrate that emodin attenuates pathological hypertrophy in female mice. Future research is needed to dissect if changes in the microbiome contributes to emodin-mediated attenuation in cardiac remodeling.
有证据表明，食物生物活性物质会影响表观基因组，以预防病理性心肌肥厚。最近，我们发现大黄素（一种蒽醌类化合物）可减轻病理性心肌肥厚和组蛋白去乙酰化酶（HDAC）活性。然而，我们仅检查了大黄素母体化合物的心脏保护作用，而没有检查大黄素代谢物或大黄素-肠道微生物组相互作用的心脏保护作用。微生物组已成为代谢和心脏等慢性病的关键因素。因此，我们假设大黄素可以逆转高血压引起的微生物群落变化。
将正常血压（血管紧张素 II）和高血压（血管紧张素 II）C57/BL6 雌性小鼠随机分为接受 vehicle（Veh；DMSO：PEG1:1）或大黄素（Emod；30mg/kg）治疗 14 天的组。在治疗前后收集体重，通过尾套测量血压。在研究结束时，处死小鼠并测量心脏重量。此外，收集粪便样本和盲肠内容物，使用 16S rRNA 测序阐明微生物种群的变化。最后，组织裂解，分离 RNA 进行 qPCR。除非另有说明，否则进行单向方差分析和 Tukey 事后检验， < 0.05 被认为具有统计学意义。
大黄素可显著减轻雌性小鼠的心肌肥厚。高血压或大黄素对体重或收缩压均无明显影响。最后，分析表明高血压改变了盲肠和盲肠内容物中的微生物组，有额外的证据支持大黄素影响粪便和结肠中的肠道微生物组。
我们的数据表明，大黄素可减轻雌性小鼠的病理性肥大。需要进一步的研究来阐明微生物组的变化是否有助于大黄素介导的心脏重构减轻。
