Evidence map›Paper›PMID 31931832›Full record

ArticleJournal of neuroinflammation2020

BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis.

Honglu Ding, Jialiang Chen, Minzhi Su, Zhijun Lin, Hailun Zhan, Fei Yang, Wenbiao Li, Juncong Xie, Yong Huang, Xianguo Liu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 160 citations in OpenAlex.

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  20. EGR2 maintains neuropathic pain by promoting microglial phagocytosis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article

32 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Honglu DingDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Jialiang ChenDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Minzhi SuDepartment of Rehabilitation, The Third Affiliated Hospital and Lingnan Hospital of the Sun Yat-Sen University, 2693 Kaichuang Rd, Guangzhou, 510700, China.
Zhijun LinDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Hailun ZhanDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Fei YangDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Wenbiao LiDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Juncong XieDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Yong HuangDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China.
Xianguo LiuPain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Rd. 2, Guangzhou, 510080, China.
Bolong LiuDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China. liubolong.happy@163.com.
Xiangfu ZhouDepartment of Urology, the Third Affiliated hospital of Sun Yat-Sen University, 600 Tianhe Rd, Guangzhou, 510630, China. xiangfuzhou1962@163.com.ORCID http://orcid.org/0000-0002-7223-6691
Sun Yat-sen University · CN

Funding

Medical Science and Technology Foundation of Guangdong Province A2017365National Natural Science Foundation of China 81670688National Natural Science Foundation of China 81800666Natural Science Foundation of Guangdong Province 2016A030313192Natural Science Foundation of Guangdong Province (CN) 2017A030310414Natural Science Foundation of Guangdong Province (CN) 2018A0303130330Youth Teacher Cultivation Project of Sun Yat-sen University 19ykpy33
6 · The paper itself

Abstract

backgroundPatients with interstitial cystitis/bladder pain syndrome (IC/BPS) often grieve over a low quality of life brought about by chronic pain. In our previous studies, we determined that neuroinflammation of the spinal dorsal horn (SDH) was associated with mechanisms of interstitial cystitis. Moreover, it has been shown that brain-derived neurotrophic factor (BDNF) participates in the regulation of neuroinflammation and pathological pain through BDNF-TrkB signaling; however, whether it plays a role in cyclophosphamide (CYP)-induced cystitis remains unclear. This study aimed to confirm whether BDNF-TrkB signaling modulates neuroinflammation and mechanical allodynia in CYP-induced cystitis and determine how it occurs.

methodsSystemic intraperitoneal injection of CYP was performed to establish a rat cystitis model. BDNF-TrkB signaling was modulated by intraperitoneal injection of the TrkB receptor antagonist, ANA-12, or intrathecal injection of exogenous BDNF. Mechanical allodynia in the suprapubic region was assessed using the von Frey filaments test. The expression of BDNF, TrkB, p-TrkB, Iba1, GFAP, p-p38, p-JNK, IL-1β, and TNF-α in the L6-S1 SDH was measured by Western blotting and immunofluorescence analysis.

resultsBDNF-TrkB signaling was upregulated significantly in the SDH after CYP was injected. Similarly, the expressions of Iba1, GFAP, p-p38, p-JNK, IL-1β, and TNF-α in the SDH were all upregulated. Treatment with ANA-12 could attenuate mechanical allodynia, restrain activation of astrocytes and microglia and alleviate neuroinflammation. Besides, the intrathecal injection of exogenous BDNF further decreased the mechanical withdrawal threshold, promoted activation of astrocytes and microglia, and increased the release of TNF-α and IL-1β in the SDH of our CYP-induced cystitis model.

conclusionsIn our CYP-induced cystitis model, BDNF promoted the activation of astrocytes and microglia to release TNF-α and IL-1β, aggravating neuroinflammation and leading to mechanical allodynia through BDNF-TrkB-p38/JNK signaling.

Indexed as

AnimalsAstrocytesBrain-Derived Neurotrophic FactorCyclophosphamideCystitisFemaleHyperalgesiaImmunosuppressive AgentsInflammationMicrogliaRatsRats, Sprague-DawleySignal TransductionSpinal Cord Dorsal HornBdnf protein, ratBrain-Derived Neurotrophic FactorCyclophosphamideImmunosuppressive AgentsAstrocytesBDNFCystitisMechanical allodyniaMicrogliaNeuroinflammationTrkB

Identifiers

PMID31931832
PMCPMC6958761
OpenAlexW3004772127

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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.