Evidence map›Paper›PMID 26307750›Full record

ArticleInflammation2016

Icariin Attenuates High-cholesterol Diet Induced Atherosclerosis in Rats by Inhibition of Inflammatory Response and p38 MAPK Signaling Pathway.

Yanwu Hu, Bo Sun, Kai Liu, Mengtong Yan, Yang Zhang, Chunsheng Miao, Liqun Ren

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
8.4field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Yanwu HuDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Bo SunDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Kai LiuDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Mengtong YanDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Yang ZhangDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Chunsheng MiaoDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China.
Liqun RenDepartment of Experimental Pharmacology and Toxicology, School of Medicine, Jilin University, Fujin Road 1266, Changchun, Jilin, 130021, People's Republic of China. renlqjlu@163.com.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Icariin is a flavonoid isolated from the traditional Chinese herbal medicine Epimedium brevicornum Maxim and has been reported to be effective for the treatment of a variety of cardiovascular diseases. The aim of the present study was to investigate the effect and mechanism of icariin on atherosclerosis (AS) using a high-cholesterol diet (HCD)-induced rat model. Seventy male Wistar rats were divided into five groups: 20 in the control group, 20 in the AS group, 10 in the simvastatin group, 10 in the low-dose icariin group, and 10 in the high-dose icariin group. A HCD and vitamin D3 were administered to establish AS rat model. The five groups of rats received daily intragastric administration of normal saline, simvastatin, or icariin (30 mg/kg/d, 60 mg/kg/d) for 4 weeks. The levels of blood lipids, superoxide dismutase (SOD), and malonaldehyde (MDA) were measured. The mRNA levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were analyzed by real-time RT-PCR, and the serum levels of IL-6 and TNF-α were measured using ELISA kit. In addition, the expression of phosphorylated p38 (p-p38) MAPK was detected by Western blot analysis. The results indicated that AS rat models were successfully constructed. In the AS group, the levels of blood lipids including total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), and MDA were significantly increased, while high-density lipoprotein-cholesterol (HDL-C) and SOD were significantly decreased, compared with those in the control group. However, icariin succeeded in improving these biochemical parameters towards the normal values in the control group. In the simvastatin group and the icariin groups, the serum levels of IL-6 and TNF-α and the related tissue mRNA levels, as well as the expression of p-p38 MAPK, were markedly reduced compared with the AS group. In conclusion, the present study indicated that icariin inhibited the HCD-induced dyslipidemia in rats, the mechanisms may be associated with the anti-inflammation, anti-oxidative stress, and downregulation of p-p38 MAPK by icariin.

Indexed as

AnimalsAnticholesteremic AgentsAtherosclerosisCholesterolCholesterol, HDLCholesterol, LDLDiet, High-FatDisease Models, AnimalDown-RegulationDrugs, Chinese HerbalDyslipidemiasFlavonoidsInflammationInterleukin-6LipidsMaleAnticholesteremic AgentsCholesterolCholesterol, HDLCholesterol, LDLDrugs, Chinese HerbalFlavonoidsicariinInterleukin-6LipidsMalondialdehydep38 Mitogen-Activated Protein KinasesRNA, MessengerSimvastatinSuperoxide DismutaseTriglyceridesTumor Necrosis Factor-alphaatherosclerosisdyslipidemiaicariininflammationoxidative stressp38 MAPK

Identifiers

PMID26307750
OpenAlexW1168383324

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

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.