Evidence map›Paper›PMID 30770640›Full record

ArticleJournal of cellular and molecular medicine2019

Ligustilide attenuates nitric oxide-induced apoptosis in rat chondrocytes and cartilage degradation via inhibiting JNK and p38 MAPK pathways.

Yan Zhou, Jianghua Ming, Yaming Li, Ming Deng, Qing Chen, Yonggang Ma, Zhonghui Chen, Yubiao Zhang, Shiqing Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.7field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

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  2. Pharmaceuticals (Basel, Switzerland) · 2026
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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

9 authors at 1 institution in 1 country.

Yan ZhouDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0003-1529-8746
Jianghua MingDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yaming LiDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Ming DengDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Qing ChenDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yonggang MaDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Zhonghui ChenDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yubiao ZhangDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Shiqing LiuDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ligustilide (LIG) is the main lipophilic component of the Umbelliferae family of pharmaceutical plants, including Radix angelicae sinensis and Ligusticum chuanxiong. LIG shows various pharmacological properties associated with anti-inflammation and anti-apoptosis in several kinds of cell lines. However, the therapeutic effects of LIG on chondrocyte apoptosis remain unknown. In this study, we investigated whether LIG had an anti-apoptotic activity in sodium nitroprusside (SNP)-stimulated chondrocyte apoptosis and could delay cartilage degeneration in a surgically induced rat OA model, and elucidated the potential mechanisms. In vitro studies revealed that LIG significantly suppressed chondrocyte apoptosis and cytoskeletal remodelling, which maintained the nuclear morphology and increased the mitochondrial membrane potential. In terms of SNP, LIG treatment considerably reduced the expression levels of cleaved caspase-3, Bax and inducible nitric oxide synthase and increased the expression level of Bcl-2 in a dose-dependent manner. The LIG-treated groups presented a significantly suppressed expression of activating transcription factor 2 and phosphorylation of Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). The inhibitory effect of LIG was enhanced by the p38 MAPK inhibitor SB203580 or the JNK inhibitor SP600125 and offset by the agonist anisomycin. In vivo studies demonstrated that LIG attenuated osteoarthritic cartilage destruction by inhibiting the cartilage chondrocyte apoptosis and suppressing the phosphorylation levels of activating transcription factor 2, JNK and p38 MAPK. This result was confirmed by histological analyses, micro-CT, TUNEL assay and immunohistochemical analyses. Collectively, our studies indicated that LIG protected chondrocytes against SNP-induced apoptosis and delayed articular cartilage degeneration by suppressing JNK and p38 MAPK pathways.

Indexed as

4-ButyrolactoneAnimalsApoptosisCartilage, ArticularCell Nucleus ShapeCell SurvivalChondrocytesDisease Models, AnimalEnzyme ActivationInjections, Intra-ArticularJNK Mitogen-Activated Protein KinasesMaleMembrane Potential, MitochondrialNitric OxideNitroprussideOsteoarthritis4-ButyrolactoneJNK Mitogen-Activated Protein KinasesligustilideNitric OxideNitroprussidep38 Mitogen-Activated Protein KinasesapoptosisJNKligustilideosteoarthritisp38 MAPK

Identifiers

PMID30770640
PMCPMC6484328
OpenAlexW2913535172

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Registered trials

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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.