Evidence map›Paper›PMID 34626306›Full record

ArticleNeurochemical research2022

Salidroside Alleviates Chronic Constriction Injury-Induced Neuropathic Pain and Inhibits of TXNIP/NLRP3 Pathway.

Tingting Hu, Qingyu Sun, Yu Gou, Yurui Zhang, Yumeng Ding, Yiran Ma, Jing Liu, Wen Chen, Ting Lan, Peipei Wang and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 18 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

12 authors at 2 institutions in 1 country.

Tingting HuDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Qingyu SunDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Yu GouDepartment of Orthopaedic Surgery, Tianjin Hospital, Tianjin University, Tianjin, China.
Yurui ZhangDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Yumeng DingDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Yiran MaDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Jing LiuDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Wen ChenDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Ting LanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, China.
Peipei WangDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China.
Qian LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, China.
Fei YangDepartment of Neurobiology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, Fengtai District, Beijing, 100069, China. feiyang@ccmu.edu.cn.ORCID http://orcid.org/0000-0003-3122-2960
Capital Medical University · CNTianjin University · CN

Funding

Beijing Natural Science Foundation Program and Scientific Research Key Program of Beijing Municipal Commission of Education KZ201910025026National Natural Science Foundation of China No. 81971037
6 · The paper itself

Abstract

Neuropathic pain is one of the most common conditions requiring treatment worldwide. Salidroside (SAL), a phenylpropanoid glucoside extracted from Rhodiola, has been suggested to produce an analgesic effect in chronic pain. However, whether SAL could alleviate pain hypersensitivity after peripheral nerve injury and its mode of action remains unclear. Several studies suggest that activation of the spinal NOD-like receptor protein 3 (NLRP3) inflammasome and its related proteins contribute to neuropathic pain's pathogenesis. This study investigates the time course of activation of spinal NLRP3 inflammasome axis in the development of neuropathic pain and also whether SAL could be an effective treatment for this type of pain by modulating NLRP3 inflammasome. In the chronic constriction injury (CCI) mice model, spinal NLRP3 inflammasome-related proteins and TXNIP, the mediator of NLRP3, were upregulated from the 14th to the 28th day after injury. The TXNIP and NLRP3 inflammasome-related proteins were mainly present in neurons and microglial cells in the spinal dorsal horn after CCI. Intraperitoneal injection of SAL at 200 mg/kg for 14 consecutive days starting from the 7th day of CCI injury could ameliorate mechanical and thermal hypersensitivity in the CCI model. Moreover, SAL inhibited the activation of the TXNIP/NLRP3 inflammasome axis and mitigated the neuronal loss of spinal dorsal horn induced by nerve injury. These results indicate that SAL could produce analgesic and neuroprotective effects in the CCI model of neuropathic pain.

Indexed as

NeuralgiaNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCarrier ProteinsCell Cycle ProteinsConstrictionGlucosidesInflammasomesMiceNLR ProteinsPhenolsRatsRats, Sprague-DawleyThioredoxinsCarrier ProteinsCell Cycle ProteinsGlucosidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseNlrp3 protein, ratNLR ProteinsPhenolsrhodiolosideThioredoxinsTxnip protein, mouseTXNIP protein, ratNeuropathic painNLRP3 inflammasomeSalidrosideSpinal cordTXNIP

Identifiers

PMID34626306
OpenAlexW3204239479

What OpenQuestion holds

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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.