Evidence map›Paper›PMID 32010290›Full record

ArticleExperimental and therapeutic medicine2020

Saikosaponin a attenuates hyperlipidemic pancreatitis in rats via the PPAR-γ/NF-κB signaling pathway.

Pingping Feng, Yanfang Xu, Baoyan Tong, Xiaoqun Tong, Yinyan Bian, Shufen Zhao, Hongbo Shen

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 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 2 institutions in 1 country.

Pingping FengDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Yanfang XuDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Baoyan TongDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Xiaoqun TongDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Yinyan BianDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Shufen ZhaoDepartment of Digestion, Lin'an District Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311300, P.R. China.
Hongbo ShenDepartment of Hepatobiliary Surgery, Quzhou People's Hospital, Quzhou, Zhejiang 324000, P.R. China.
Hangzhou Hospital of Traditional Chinese Medicine · CNQuzhou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic effect of saikosaponin a (SSa) on hyperlipidemic pancreatitis (HP) is not completely understood. The aim of the present study was to investigate the therapeutic effect and the underlying mechanism of SSa using a rat model of HP. Following successful establishment of the HP rat model, different doses of SSa (low dose group, 10 mg/kg or high dose group, 20 mg/kg) were administrated. Histopathological examination, the wet/dry (W/D) ratio and myeloperoxidase (MPO) activity of the pancreatic tissues were assessed. The lipid, amylase (AMY), lipase and proinflammatory cytokine profiles in serum, as well as the expression of peroxisome proliferator-activated receptor (PPAR)-γ and the NF-κB signaling pathway-related proteins in pancreatic tissues were evaluated. The results showed that SSa effectively attenuated pancreatic pathological injury and reduced both the W/D ratio and MPO activity compared to the HP model rats. SSa also improved lipid metabolism by significantly decreasing the serum levels of total cholesterol and triglycerides (P<0.05). Following the administration of SSa, the activity of AMY and lipase, as well as the levels of the proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β and IL-6 were reduced, particularly in the high dosage group (P<0.05). Furthermore, SSa activated PPAR-γ expression and suppressed the NF-κB signaling pathway in pancreatic tissues. The present study suggested that SSa attenuated HP in rats by increasing lipid metabolism and inhibiting the release of proinflammatory cytokines via the NF-κB inflammatory pathway. The results from the present study indicated that SSa might be a promising therapeutic agent for the treatment of HP.

Indexed as

hyperlipidemiaNF-κBpancreatitisperoxisome proliferator-activated receptor-γsaikosaponin a

Identifiers

PMID32010290
PMCPMC6966209
OpenAlexW2995223847

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.