Evidence map›Paper›PMID 31719257›Full record

ArticleNeural regeneration research2020

Expression and effect of sodium-potassium-chloride cotransporter on dorsal root ganglion neurons in a rat model of chronic constriction injury.

Chao-Yang Tan, Yan-Ping Wang, Yuan-Yuan Han, Bi-Han Lu, Wei Ji, Li-Cang Zhu, Yang Wang, Wen-Yan Shi, Li-Ya Shan, Liang Zhang and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 19 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

13 authors at 3 institutions in 1 country.

Chao-Yang TanDepartment of Physiology, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region; Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang Province; Department of Health, Karamay Army Division, Chinese People's Liberation Army, Karamay, Xinjiang Uygur Autonomous Region, China.
Yan-Ping WangDepartment of Physiology; Department of Nursing, Medical College of Jiaxing University, Jiaxing, Zhejiang Province, China.
Yuan-Yuan HanDepartment of Physiology, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region; Department of Clinical Medicine, Karamay College of Xinjiang Medical University, Karamay, Xinjiang Uygur Autonomous Region, China.
Bi-Han LuDepartment of Physiology, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Wei JiDepartment of Physiology, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Li-Cang ZhuDepartment of Neurosurgery, First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Yang WangDepartment of Physiology, College of Medicine; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Wen-Yan ShiDepartment of Physiology, College of Medicine; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Li-Ya ShanDepartment of Physiology, College of Medicine; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Liang ZhangDepartment of Physiology, College of Medicine; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Ke-Tao MaDepartment of Physiology, College of Medicine; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Li LiDepartment of Physiology, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region; Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang Province; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region, China.
Jun-Qiang SiDepartment of Physiology; The key Laboratory of Xinjiang Endemic and Ethnic Diseases, College of Medicine, Shihezi University, Shihezi, Xinjiang Uygur Autonomous Region; Department of Physiology, School of Basic Medical Sciences, Wuhan University; Department of Physiology, School of Basic Medical Sciences, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Shihezi University · CNFirst Affiliated Hospital of Shihezi University Medical College · CNJiaxing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain. We investigated whether the increase of NKCC1 and KCC2 is associated with peripheral pain transmission in dorsal root ganglion neurons. To this aim, rats with persistent hyperalgesia were randomly divided into four groups. Rats in the control group received no treatment, and the rat sciatic nerve was only exposed in the sham group. Rats in the chronic constriction injury group were established into chronic constriction injury models by ligating sciatic nerve and rats were given bumetanide, an inhibitor of NKCC1, based on chronic constriction injury modeling in the chronic constriction injury + bumetanide group. In the experiment measuring thermal withdrawal latency, bumetanide (15 mg/kg) was intravenously administered. In the patch clamp experiment, bumetanide (10 µg/µL) and acutely isolated dorsal root ganglion neurons (on day 14) were incubated for 1 hour, or bumetanide (5 µg/µL) was intrathecally injected. The Hargreaves test was conducted to detect changes in thermal hyperalgesia in rats. We found that the thermal withdrawal latency of rats was significantly decreased on days 7, 14, and 21 after model establishment. After intravenous injection of bumetanide, the reduction in thermal retraction latency caused by model establishment was significantly inhibited. Immunohistochemistry and western blot assay results revealed that the immune response and protein expression of NKCC1 in dorsal root ganglion neurons of the chronic constriction injury group increased significantly on days 7, 14, and 21 after model establishment. No immune response or protein expression of KCC2 was observed in dorsal root ganglion neurons before and after model establishment. The Cl

Indexed as

bumetanidechronic constriction injurydorsal root gangliondorsal root reflexhyperalgesiaKCC2nerve regenerationneuropathic painNKCC1primary afferent depolarizationwhole-cell patch clamp

Identifiers

PMID31719257
PMCPMC6990784
OpenAlexW2983179773

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.