Evidence map›Paper›PMID 40788369›Full record

ArticleMolecular biology reports2025

Specnuezhenide mitigates tunicamycin-induced liver injury in mice via ER stress modulation and metabolic reprogramming.

Tianle Zhang, Dan Bi, Jiahui Li, Xin Jin, Huijuan Wu, Changyuan Yang, Siping Yu, Hedong Rong, Yanhong Yang, Zili Lei

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Tianle Zhang *Institute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Dan Bi *Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, 250012, China.
Jiahui LiInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Xin JinThe First Affiliated Hospital, (School of Clinical Medicine), Guangdong Pharmaceutical University, Nong-Lin-Xia Road 19#, Yue-Xiu District, Guangzhou, 510080, P.R. China.
Huijuan WuInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Changyuan YangInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Siping YuInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Hedong RongInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China.
Yanhong YangThe First Affiliated Hospital, (School of Clinical Medicine), Guangdong Pharmaceutical University, Nong-Lin-Xia Road 19#, Yue-Xiu District, Guangzhou, 510080, P.R. China. 1764941457@qq.com.
Zili LeiInstitute of Chinese Medicine, Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorders of the Ministry of Education, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangdong Pharmaceutical University, No. 280 Wai-Huan-Dong Road, Guangzhou, 510006, China. 3182683090@qq.com.

Funding

the Guangdong Basic and Applied Basic Research Foundation 2021A1515012383the Key Field Special Project for Colleges and Universities of Guangdong Province (Biomedicine and Health) No. 2023ZDZX2030
6 · The paper itself

Abstract

backgroundDrug-induced liver injury (DILI) is a major health concern, often linked to endoplasmic reticulum (ER) stress. Specnuezhenide (SPE), a bioactive iridoid glycoside from Ligustrum lucidum, is known for its hepatoprotective effects, but its role in ER stress-mediated DILI remains unclear. This study investigated the protective mechanisms of SPE against tunicamycin (TM)-induced liver injury, focusing on ER stress and metabolic reprogramming.

methodsMale C57BL/6 mice were pretreated with SPE (40, 80, or 160 mg/kg) or the positive control 4-phenylbutyric acid (PBA) for seven days, followed by a single intraperitoneal injection of TM (1 mg/kg) to induce acute liver injury. Liver injury, lipid profiles, histopathology, ER stress markers, insulin signaling, lipid and cholesterol metabolism, and markers of inflammation and oxidative stress were evaluated.

resultsSPE pretreatment significantly alleviated TM-induced liver injury, as indicated by reduced serum ALT and AST levels, decreased liver weight, and improved hepatic histopathology. Mechanistically, SPE inhibited activation of the PERK/eIF2α/CHOP axis of the unfolded protein response (UPR), restored metabolic homeostasis by enhancing hepatic insulin sensitivity via the AKT/GSK3β/mTOR pathway, normalized lipid and cholesterol metabolism gene expression, and reduced hepatic steatosis. SPE also attenuated hepatic inflammation and oxidative stress.

conclusionsSpecnuezhenide protects against TM-induced liver injury through multiple mechanisms, including suppression of ER stress, restoration of metabolic homeostasis, and reduction of inflammation and oxidative stress. Therefore, these findings highlight SPE as a promising therapeutic candidate for DILI.

Indexed as

Chemical and Drug Induced Liver InjuryEndoplasmic Reticulum StressTunicamycinAnimalsLipid MetabolismLiverMaleMetabolic ReprogrammingMiceMice, Inbred C57BLOxidative StressProtective AgentsSignal TransductionUnfolded Protein ResponseProtective AgentsTunicamycinDrug-induced liver injuryEndoplasmic reticulum stressHepatotoxicityOxidative stressSpecnuezhenide

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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.