Evidence map›Paper›PMID 37737440›Full record

ArticleBiological trace element research2024

MAPK Signaling Pathway Plays Different Regulatory Roles in the Effects of Boric Acid on Proliferation, Apoptosis, and Immune Function of Splenic Lymphocytes in Rats.

Shuqin Chen, Haoran Fan, Yaqiong Pei, Kaihuan Zhang, Feng Zhang, Qianqian Hu, Erhui Jin, Shenghe Li

Abstract read
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In one paragraph

Article in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. The Biological Effects of Boron in Animals and Humans.Biological trace element research · 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

8 authors at 1 institution in 1 country.

Shuqin ChenCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Haoran FanCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Yaqiong PeiCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Kaihuan ZhangCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Feng ZhangCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Qianqian HuCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.
Erhui JinCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China. jineh@ahstu.edu.cn.ORCID https://orcid.org/0000-0002-5477-5317
Shenghe LiCollege of Animal Science, Anhui Science and Technology University, No.9 Donghua Road, Fengyang County, Chuzhou, Anhui Province, 233100, People's Republic of China.ORCID https://orcid.org/0000-0001-8767-6991
Anhui University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Boron is one of the essential trace elements in animals. Although boron supplementation can enhance immune function and promote cell proliferation, high-dose boron supplementation can negatively affect immune function and inhibit cell proliferation. Furthermore, its action pathway is unknown. In this study, ERK1/2, JNK, and p38MAPK signaling pathways were blocked using specific blockers to investigate the impact of low-dose and high-dose boron on proliferation, apoptosis, and immune function of lymphocytes, and the expression of genes related to cell proliferation and apoptosis in rats. The addition of 0.4 mmol/L boron did not affect the ratio of CD4+/CD8+ T cells (P>0.05), IgG and IFN-γ contents (P>0.05), the proliferation rate of lymphocytes (P>0.05), and mRNA and protein expressions of PCNA (P>0.05) in the spleen after ERK1/2 signal pathway was selectively inhibited. Moreover, the addition of 40 mmol/L boron did not affect the proportion of CD4+ T cells, contents of IgG and cytokines (IL-2 and IL-4), proliferation and apoptosis rates of lymphocytes, and expression of proliferation- and apoptosis-related genes in the spleen. Meanwhile, the addition of 0.4 mmol/l boron increased the ratio of CD4+/CD8+ T cells (P<0.05 or P<0.01), IFN-γ or IgG contents (P<0.05), and the proliferation rate of lymphocytes (P<0.05) in spleen after selective inhibition of JNK or p38MAPK signaling pathways, while the protein expression of Caspase-3 decreased (P<0.05 or P<0.01). Furthermore, 40 mmol/L boron decreased the proportion of lymphocyte subsets, cytokine contents, proliferation rate of lymphocytes, and mRNA and protein expressions of PCNA. In contrast, the mRNA and protein expressions of Caspase-3 and protein expression of Bax were increased. These results indicate that ERK1/2 signaling pathway mainly regulates the effects of low-dose and high-dose boron on proliferation, apoptosis, and immune function of splenic lymphocytes.

Indexed as

ApoptosisCell ProliferationLymphocytesMAP Kinase Signaling SystemSpleenAnimalsMaleRatsRats, Sprague-DawleyBoronCell proliferation and apoptosisCytokineMAPK signaling pathwaySplenic lymphocytes

Identifiers

PMID37737440
OpenAlexW4386945385

What Socratic holds

Textmetadata
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 Socratic graph.