Evidence map›Paper›PMID 36118100›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2022

Protective Effect of Shengmaiyin in Myocardial Hypertrophy-Induced Rats: A Genomic Analysis by 16S rDNA.

Sitong Ming, Mo Kan, Liu Liu, Zhuang Zhang, Xiaoran Liu, Yaxin Liu, Zhen Li, Yanhong Zhang, Qihang Pang, Jianan Lin and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The potential of medicinal food plantFrontiers in pharmacology · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 1 institution in 1 country.

Sitong MingJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0001-5455-5982
Mo KanJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Liu LiuJilin Province Drug Evaluation Center, Changchun, Jilin 130062, China.
Zhuang ZhangJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0002-7642-0082
Xiaoran LiuJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0002-4223-357X
Yaxin LiuJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Zhen LiJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Yanhong ZhangJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Qihang PangJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Jianan LinJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Hui LiQian Wei Hospital of Jilin Province, Changchun, Jilin 130012, China.
Qing YangJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.
Xin SuiJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0003-4465-9686
Xiaobo QuJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0002-2651-4822
Na LiJilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130021, China.ORCID https://orcid.org/0000-0002-9383-3049
Changchun University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The gut-cardiac axis theory provides new insights into the complex mechanisms of cardiac hypertrophy and provides new therapeutic targets. Cardiac hypertrophy is a risk factor for heart failure. Shengmaiyin (SMY) is a traditional Chinese medicine formula with clear effects in the treatment and prevention of cardiac hypertrophy, but the mechanism by which it improves cardiac hypertrophy is still unclear. Therefore, this study aimed to investigate the protective effect and mechanism of SMY on isoproterenol (ISO)-induced myocardial hypertrophy in rats. Methods: First, various pharmacodynamic methods were used to evaluate the therapeutic effect of SMY on ISO-induced myocardial hypertrophy in rats. Then, 16S rDNA amplicon sequencing technology was used to study the effect of SMY on the intestinal flora of rats with myocardial hypertrophy. Finally, the mechanism underlying the effect of SMY on cardiac hypertrophy was predicted by bioinformatics network analysis and verified by Western blotting. Results: SMY increased ejection fraction (EF%) and left ventricular fractional shortening (FS%), ameliorated myocardial cell injury and fibrosis, regulated blood lipids and energy metabolism, and decreased cardiac hypertrophy marker gene expression. The gut microbiota of ISO-induced myocardial hypertrophy rats were significantly changed, while SMY effectively ameliorated the dysbiosis of the intestinal flora in rats with myocardial hypertrophy, especially Conclusion: SMY significantly improves cardiac function, relieves myocardial cell fibrosis and necrosis, resists cardiac hypertrophy, improves blood lipid metabolism and energy metabolism, regulates intestinal microbial disturbance, and protects the heart.

Identifiers

PMID36118100
PMCPMC9473885
OpenAlexW4296001824

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.