RNA-Seq analysis of improving mechanism for cardiac hypertrophy of a propolis product

Authors

SUN Yanru, College of Life Science, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, China; College of Bee Science, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, China; National United Engineering Laboratory of Natural Biologic
HAN Mingfeng, National United Engineering Laboratory of Natural Biological Toxins, Fuzhou, Fujian 350002, China
SHEN Zhenhuang, National United Engineering Laboratory of Natural Biological Toxins, Fuzhou, Fujian 350002, China
WU Zhenhong, College of Bee Science, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, China; National United Engineering Laboratory of Natural Biological Toxins, Fuzhou, Fujian 350002, China
MIAO Xiaoqing, College of Bee Science, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, China; National United Engineering Laboratory of Natural Biological Toxins, Fuzhou, Fujian 350002, China

Abstract

To study the improving mechanism of a propolis product on cardiac hypertrophy, spontaneously hypertensive rats (SHRs) were picked as animal models.After continuous infusion of this propolis product for 35 d, left ventricular index were calculated and RNA-Seq was performed. Differentially expressed genes (DEGs) were screened with the following GO enrichment analysis and KEGG metabolic pathway analysis. Totally 1 297 DEGs (91 DEGs were up-regulated and 1 206 DEGs were down-regulated) were selected. Results of KEGG metabolic pathways showed that 410 DEGs were enriched into 182 KEGG pathways, among which the top three DEGs enrichment is closely related to insulin signal transduction pathways, namely PI3K-Akt signaling pathway, insulin signaling pathway and MAPK signal pathway. It was indicated that the effect of the propolis product on the myocardial hypertrophy of SHRs was improved and the main KEGG pathways were associated with insulin signal transduction.

Publication Date

1-28-2018

First Page

17

Last Page

22

DOI

10.13652/j.issn.1003-5788.2018.01.004

Recommended Citation

Yanru, SUN; Mingfeng, HAN; Zhenhuang, SHEN; Zhenhong, WU; and Xiaoqing, MIAO (2018) "RNA-Seq analysis of improving mechanism for cardiac hypertrophy of a propolis product," Food and Machinery: Vol. 34: Iss. 1, Article 4.
DOI: 10.13652/j.issn.1003-5788.2018.01.004
Available at: https://www.ifoodmm.cn/journal/vol34/iss1/4

References

[1] MENSAH G A, CROFT J B, GILES W H. The heart, kidney, and brain as target organs in hypertension[J]. Curr Probl Cardiol, 2003, 28(2): 156-193.
[2] KATHOLI R E, COURI D M. Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications[J]. International Journal of Hypertension, 2011, 2 011: 1-10.
[3] SCHIRONE L, FORTE M, PALMERIO S, et al. A review of the molecular mechanisms underlying the development and progression of cardiac remodeling[J]. Oxidative Medicine and Cellular Longevity, 2017, 2 017: 3 920 195.
[4] 刘丽娜, 李法琦. 心肌肥厚相关信号通路的研究进展[J]. 重庆医学, 2010(20): 2 805-2 808.
[5] 张勇涛, 蒋凡. 生理性和病理性心肌肥厚的信号传导机制[J]. 中华心血管病杂志, 2015, 43(3): 277-280.
[6] 徐洋, 李强, 侯化化, 等. 异钩藤碱通过下调CaN、ERK2和上调MKP-1的表达抑制大鼠心肌细胞肥大[J] . 遵义医学院学报, 2013, 36(3): 210-217.
[7] 吴赛, 姜月华, 杨传华, 等. 半夏白术天麻汤对痰湿壅盛型高血压大鼠心肌MAPK信号通路的影响[J]. 中国实验方剂学杂志, 2016(8): 159-165.
[8] 叶强, 陈良海, 刘应才, 等. 辛伐他汀通过Akt/GSK3β通路抑制心肌梗死后心肌细胞凋亡[J]. 中国药理学通报, 2011(12): 1 656-1 660.
[9] 薛一涛, 陈炜, 刘鹏, 等. 复心汤对心力衰竭大鼠PI3K-Akt-GSK3β通路的影响[J]. 上海中医药杂志, 2015(8): 74-78.
[10] 刘婕, 高虹, 缪晓青. 宝元灵对离体蛙心脏收缩功能的影响[J]. 华西药学杂志, 2014(2): 140-142.
[11] LIU Jie, GAO Hong, FU Ming-ju, et al. Therapeutical efficacy of bee venom compound preparation bao yuan ling on rats with chronic heart failure[J]. Journal of Animal and Veterinary Advances, 2014, 13(13): 801-806.
[12] TRIPPODO N, FROHLICH E. Similarities of genetic (spontaneous) hypertension. Man and rat[J]. Circulation Research, 1981, 48(3): 309-319.
[13] FROHLICH E D. Is the spontaneously hypertensive rat a model for human hypertension?[J]. Journal of Hypertension Supplement Official Journal of the International Society of Hypertension, 1986, 4(4): S15-S19.
[14] MUTLAK M, KEHAT I. Extracellular signal-regulated kinases 1/2 as regulators of cardiac hypertrophy[J]. Frontiers in Pharmacology, 2015, doi: 10.3389/fphar.2015.00149.
[15] 程杰坤, 孙小慧, 高莉萍, 等. 法舒地尔对异丙肾上腺素诱导大鼠心肌肥厚的干预作用及其机制[J]. 中国应用生理学杂志, 2016, 32(5): 414-418.
[16] RIEHLE C, ABEL E D. Insulin Signaling and Heart Failure[J]. Circulation Research, 2016, 118(7): 1 151-1 169.
[17] 范婷婷, 刘琼. 姜黄素对脂多糖诱导的心肌功能障碍小鼠PI3K-γ表达的影响[J]. 重庆医科大学学报, 2014(10): 1 368-1 372.
[18] MICHAEL A, HAQ S, CHEN Xin, et al. Glycogen synthase kinase-3β regulates growth, calcium homeostasis, and diastolic function in the heart[J]. Journal of Biological Chemistry, 2004, 279(20): 21 383-21 393.
[19] SUGDEN P, FULLER S, WEISS S, et al. Glycogen synthase kinase 3 (GSK3) in the heart: a point of integration in hypertrophic signalling and a therapeutic target? A critical analysis[J]. British Journal of Pharmacology, 2008, 153: S137-S153.