Evidence map›Paper›PMID 35840932›Full record

ArticleBMC complementary medicine and therapies2022

Ginsenoside Rg3 induces apoptosis and inhibits proliferation by down-regulating TIGAR in rats with gastric precancerous lesions.

Shangbin Lv, Xiaodong Chen, Yu Chen, Daoyin Gong, Gang Mao, Caifei Shen, Ting Xia, Jing Cheng, Zhaoliang Luo, Yu Cheng and 2 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC complementary medicine and therapies, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Shangbin Lv *Basic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Xiaodong Chen *Department of Gastrointestinal Surgery, Sichuan Cancer Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Yu Chen *Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Daoyin GongHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Gang MaoHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Caifei ShenDigestive Endoscopy Center, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Ting XiaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jing ChengChengdu University of Traditional Chinese Medicine, Chengdu, China.
Zhaoliang LuoBasic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Yu ChengSichuan University West China Hospital Ganzi Hospital, Ganzi, China.
Weihong LiBasic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, China. lwh@cdutcm.edu.cn.
Jinhao ZengDepartment of Chinese Internal Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China. zengjinhao@cdutcm.edu.cn.
Chengdu University of Traditional Chinese Medicine · CNUniversity of Electronic Science and Technology of China · CNWest China Hospital of Sichuan University · CN

Funding

"Hundred Talents Program" of the Hospital of Chengdu University of Traditional Chinese Medicine 21-Y17National Natural Science Foundation of China 81804066Project of Sichuan Administration of traditional Chi- nese Medicine 2021MS104Xinglin Scholar Research Promotion Project of Chengdu University of TCM QNXZ2019017
6 · The paper itself

Abstract

backgroundGinsenoside Rg3 (GRg3) is one of the main active ingredients in Chinese ginseng extract and has various biological effects, such as immune-enhancing, antitumour, antiangiogenic, immunomodulatory and anti-inflammatory effects. This study aimed to investigate the therapeutic effect of GRg3 on gastric precancerous lesion (GPL) induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and the potential mechanism of action.

methodsThe MNNG-ammonia composite modelling method was used to establish a rat model of GPL. Histopathological changes in the rat gastric mucosa were observed by pathological analysis using haematoxylin-eosin staining to assess the success rate of the composite modelling method. Alcian blue-periodic acid Schiff staining was used to observe intestinal metaplasia in the rat gastric mucosa. Apoptosis was detected in rat gastric mucosal cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling staining. The production level of reactive oxygen species (ROS) was determined by the dihydroethidium fluorescent probe method, and that of TP53-induced glycolysis and apoptosis regulator (TIGAR) protein was determined by immunohistochemical staining and western blotting. The production levels of nicotinamide adenine dinucleotide phosphate (NADP) and glucose-6-phosphate dehydrogenase (G6PDH) were determined by an enzyme-linked immunosorbent assay, and that of glutathione (GSH) was determined by microanalysis.

resultsGRg3 significantly alleviated the structural disorganization and cellular heteromorphism in the form of epithelial glands in the gastric mucosa of rats with GPL and retarded the progression of the disease. Overexpression of TIGAR and overproduction of NADP, GSH and G6PDH occurred in the gastric mucosal epithelium of rats with GPL, which in turn led to an increase in the ROS concentration. After treatment with GRg3, the expression of TIGAR and production of NADP, GSH G6PDH decreased, causing a further increase in the concentration of ROS in the gastric mucosal epithelium, which in turn induced apoptosis and played a role in inhibiting the abnormal proliferation and differentiation of gastric mucosal epithelial cells.

conclusionGrg3 can induce apoptosis and inhibit cell proliferation in MNNG-induced GPL rats. The mechanism may be related to down-regulating the expression levels of TIGAR and production levels of GSH, NADP and G6PD, and up-regulating the concentration of ROS.

Indexed as

MethylnitronitrosoguanidinePrecancerous ConditionsAnimalsApoptosisApoptosis Regulatory ProteinsCell ProliferationGinsenosidesGlycolysisNADPRatsRats, Sprague-DawleyReactive Oxygen SpeciesApoptosis Regulatory Proteinsginsenoside Rg3GinsenosidesMethylnitronitrosoguanidineNADPReactive Oxygen SpeciesApoptosisGastric precancerous lesionsGinsenoside Rg3Reactive oxygen speciesTP53-induced glycolysis and apoptosis regulator

Identifiers

PMID35840932
PMCPMC9284801
OpenAlexW4285589991

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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.