Evidence map›Paper›PMID 25206431›Full record

ArticleNeural regeneration research2013

Curcumin ameliorates hippocampal neuron damage induced by human immunodeficiency virus-1.

Hongmei Tang, Rui Pan, Wenli Fang, Yanyan Xing, Dexi Chen, Xiaobao Chen, Yuanyuan Yu, Junbing Wang, Zheng Gong, Guoyin Xiong and 1 more

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

Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact, top 88% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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

11 authors at 3 institutions in 2 countries.

Hongmei TangDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
Rui PanDepartment of Orthopedics, First Affiliated Hospital, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China.
Wenli FangDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China.
Yanyan XingDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
Dexi ChenSTD/AIDS Research Lab, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.
Xiaobao ChenDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China.
Yuanyuan YuDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China.
Junbing WangDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
Zheng GongDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
Guoyin XiongDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
Jun DongDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Institute of Brain Research, Medical College of Jinan University, Guangzhou 510632, Guangdong Province, China ; Joint Laboratory for Brain Function and Health of Jinan University and the University of Hong Kong, Guangzhou 510632, Guangdong Province, China.
University of Hong Kong · HKCapital Medical University · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous studies have shown that infection with the gp120 V3 loop can cause human immunodeficiency virus-1 associated neurocognitive disorders. Curcumin has been shown to improve these effects to some degree, but the precise mechanisms remain unknown. The present study analyzed the neuroprotective effect and mechanism of curcumin in relation to hippocampal neurons. Results showed that 1 nmol/L gp120 V3 loop suppressed the growth of synapses. After administration of 1 μmol/L curcumin, synaptic growth improved. Curcumin is neuroprotective against gp120 V3 loop-induced neuronal damage by inhibiting the activation of L-type calcium currents, relieving intracellular Ca(2+) overload, promoting Bcl-2 expression, and inhibiting Bax activation. The effect of curcumin was identical to nimodipine, suggesting that curcumin has the same neuroprotective effects against gp120 V3 loop-induced neuronal damage.

Indexed as

apoptosisCa2+curcumingp120 V3 loopgrants-supported paperhuman immunodeficiency virus-1 associated neurocognitive disordersneural regenerationneuroregenerationsynapsetraditional Chinese medicine

Identifiers

PMID25206431
PMCPMC4107768
OpenAlexW2254885894

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.