Evidence map›Paper›PMID 26664046›Full record

ArticleDrug design, development and therapy2015

Timosaponin B-II ameliorates diabetic nephropathy via TXNIP, mTOR, and NF-κB signaling pathways in alloxan-induced mice.

Yong-Liang Yuan, Chang-Run Guo, Ling-Ling Cui, Shi-Xia Ruan, Chun-Feng Zhang, De Ji, Zhong-Lin Yang, Fei Li

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 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

8 authors at 2 institutions in 1 country.

Yong-Liang YuanState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
Chang-Run GuoState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
Ling-Ling CuiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
Shi-Xia RuanState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
Chun-Feng ZhangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
De JiCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Zhong-Lin YangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
Fei LiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, People's Republic of China.
China Pharmaceutical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMany synthesized drugs with clinical severe side effects have been used for diabetic nephropathy (DN) treatment. Therefore, it is urgent and necessary to identify natural and safe agents to remedy DN. Timosaponin B-II (TB-II), a major steroidal saponin constituent in Anemarrhena asphodeloides Bunge, exhibits various activities, including anti-inflammatory and hypoglycemic functions. However, the anti-DN effects and potential mechanism(s) of TB-II have not been previously reported. PURPOSE: To investigate the effect of TB-II on DN in alloxan-induced diabetic mice.

methodsTB-II was isolated and purified from A. asphodeloides Bunge using macroporous adsorption resin and preparative high-performance liquid chromatography. The effect of TB-II on DN was evaluated in alloxan-induced diabetic mice using an assay kit and immunohistochemical determination in vivo. The expression of mammalian target of rapamycin (mTOR), thioredoxin-interacting protein (TXNIP), and nuclear transcription factor-κB (NF-κB) signaling pathways was also measured using Western blot analysis.

resultsTB-II significantly decreased the blood glucose levels and ameliorated renal histopathological injury in alloxan-induced diabetic mice. In addition, TB-II remarkably decreased the levels of renal function biochemical factors, such as kidney index, blood urea nitrogen, serum creatinine, urinary uric acid, urine creatinine, and urine protein, and it reduced lipid metabolism levels of total cholesterol and triglycerides and the levels of inflammatory cytokines interleukin-6 and tumor necrosis factor-α in alloxan-induced mice. Furthermore, TB-II inhibited the expression of mTOR, TXNIP, and NF-κB.

conclusionThe results revealed that TB-II plays an important role in DN via TXNIP, mTOR, and NF-κB signaling pathways. Overall, TB-II exhibited a prominently ameliorative effect on alloxan-induced DN.

Indexed as

AlloxanAnemarrhenaAnimalsBlood GlucoseCarrier ProteinsDiabetes Mellitus, ExperimentalDiabetic NephropathiesKidneyMaleMiceMice, Inbred ICRNF-kappa BSaponinsSignal TransductionSirolimusSteroidsAlloxanBlood GlucoseCarrier ProteinsNF-kappa BSaponinsSirolimusSteroidsThioredoxinstimosaponin B-IITxnip protein, mouseAnemarrhena asphodeloides Bungediabetic nephropathymTORNF-κBtimosaponin B-IITXNIP

Identifiers

PMID26664046
PMCPMC4669930
OpenAlexW2181560749

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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.