Effects of electroacupuncture at Taichong (LR 3) and Baihui (DU 20) on cardiac hypertrophy in rats with spontaneous hypertension

J Tradit Chin Med. 2019 Aug;39(4):502-508.

Abstract

Objective: To investigate the effects of electroacupuncture (EA) at Taichong (LR 3) and Baihui (DU 20) on myocardial hypertrophy in spontaneously hypertensive rats (SHRs).

Methods: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure (SBP) and cardiac function were measured in all rats. Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR. Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.

Results: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group (P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups (P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated (P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K, Akt, and mTOR in SHRs were significantly up-regulated by EA and Losartan (P < 0.01), while the expression levels of PTEN and ANP were down-regulated (P < 0.01).

Conclusion: EA at Taichong (LR 3) and Baihui (DU 20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.

Keywords: Electroacupuncture; Hypertrophy; Mammalian target of rapamycin; Phosphatidylinositol 3-kinases; Proto-oncogene proteins c-akt; Rats, inbred SHR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acupuncture Points*
  • Animals
  • Blood Pressure
  • Cardiomegaly / genetics
  • Cardiomegaly / metabolism
  • Cardiomegaly / physiopathology
  • Cardiomegaly / therapy*
  • Electroacupuncture*
  • Humans
  • Hypertension / genetics
  • Hypertension / metabolism
  • Hypertension / physiopathology
  • Hypertension / therapy*
  • Male
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred WKY
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • MAS1 protein, human
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases