Evidence map›Paper›PMID 37076961›Full record

ArticleCurrent molecular medicine2024

CsHscB Derived from a Liver Fluke

Qian Yu, Stephane Koda, Na Xu, Jing Li, Jian-Ling Wang, Man Liu, Ji-Xin Liu, Yu Zhang, Hui-Min Yang, Bei-Bei Zhang and 5 more

Abstract read
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In one paragraph

Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

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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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

15 authors at 1 institution in 1 country.

Qian YuDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Stephane KodaDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Na XuDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Jing LiDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Jian-Ling WangDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Man LiuDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Ji-Xin LiuDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Yu ZhangDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Hui-Min YangDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Bei-Bei ZhangDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Xiang-Yang LiDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Xiao-Cui LiDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Ren-Xian TangDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Kui-Yang ZhengDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Chao YanDepartment of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, 221004, People's Republic of China.
Xuzhou Medical College · CN

Funding

National Natural Science Foundation of China 81702027Natural Science Foundation of Jiangsu Province BK20211346, BK20201011The Young Scientist of Xuzhou Medical University D2019040
6 · The paper itself

Abstract

backgroundPrimary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterized by inflammatory fibrosis usually involving the whole biliary tree. However, there are very limited treatment options to treat this disease. Our previous study found a lipid-protein rCsHscB from a liver fluke -

methodsMice were fed 0.1% DDC for 4 weeks and treated with CsHscB (30 μg/mouse, intraperitoneal injection, once every 3 days); the control group was given an equal amount of PBS or CsHscB under normal diet conditions. All the mice were sacrificed at 4 weeks for the evaluation of biliary proliferation, fibrosis, and inflammation.

resultsrCsHscB treatment attenuated DDC-induced liver congestion and enlargement and significantly decreased the upregulation of serum AST and ALT levels. The administration of rCsHscB to DDC-fed mice significantly decreased cholangiocyte proliferation and pro-inflammatory cytokine production compared to mice fed with DDC alone. Also, rCsHscB treatment showed a decreased expression of α-SMA in the liver and other markers of liver fibrosis (Masson staining, Hydroxyproline content, and collagen deposit). More interestingly, DDC-fed mice treated with rCsHscB showed a significant up-regulation of PPAR-γ expression, which was similar to control mice, indicating the involvement of PPAR-γ signaling in the protective action of rCsHscB.

conclusionOverall, our data show that rCsHscB attenuates the progression of cholestatic fibrosis induced by DDC and supports the potential for manipulating the parasite-derived molecule to treat certain immune-mediated disorders.

Indexed as

Cholangitis, SclerosingClonorchis sinensisDisease Models, AnimalLiver CirrhosisAnimalsClonorchiasisHelminth ProteinsLiverMaleMicePPAR gammaPyridines3,5-diethoxycarbonyl-1,4-dihydrocollidineHelminth ProteinsPPAR gammaPyridinesCholestatic liver fibrosisClonorchis sinensisDDCImmune regulation.PPAR-γProtein CsHscB

Identifiers

PMID37076961
OpenAlexW4366464293

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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.