Publications by authors named "Meilin Peng"

5 Publications

  • Page 1 of 1

Severe Acute Respiratory Syndrome Coronavirus 2 and Male Reproduction: Relationship, Explanations, and Clinical Remedies.

Front Physiol 2021 14;12:651408. Epub 2021 Apr 14.

Institute of Reproductive Health, Center for Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Coronavirus disease 2019 (COVID-2019) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an ongoing pandemic and worldwide public health emergency, having drawn a lot of attention around the world. The pathogenesis of COVID-19 is characterized by infecting angiotensin-converting enzyme 2 (ACE2)-expressing cells, including testis-specific cells, namely, Leydig, Sertoli, and spermatogenic cells, which are closely related to male reproduction. This leads to aberrant hyperactivation of the immune system generating damage to the infected organs. An impairment in testicular function through uncontrolled immune responses alerts more attention to male infertility. Meanwhile, the recent clinical data indicate that the infection of the human testis with SARS-CoV-2 may impair male germ cell development, leading to germ cell loss and higher immune cell infiltration. In this review, we investigated the evidence of male reproductive dysfunction associated with the infection with SARS-CoV-2 and its possible immunological explanations and clinical remedies.
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http://dx.doi.org/10.3389/fphys.2021.651408DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079781PMC
April 2021

Evaluation of 3,4,4,9-trichlorocarbanilide to zebrafish developmental toxicity based on transcriptomics analysis.

Chemosphere 2021 Sep 29;278:130349. Epub 2021 Mar 29.

Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Hubei, 430030, PR China. Electronic address:

Triclocarban (TCC), considered an endocrine-disrupting, persistent, and bioaccumulating organic matter, has attracted a great deal of attention for its pollution and health risks. However, studies on its toxicological mechanism, especially for embryo development are limited. This article explores the cardiac developmental toxicity induced in zebrafish embryos after exposure to different TCC concentrations. First, liquid chromatography-tandem mass spectrometry was used in detecting TCC in embryos in vivo after exposure to various TCC. Results showed that embryonic TCC content reached 9.23 ng after exposure to 300 μg/L TCC, the heart rates of the embryos markedly decreased, heart abnormalities significantly increased. In addition, obvious pericardial effusion was observed in the larvae. Through transcriptome sequencing, 200 differential gene expression (DGE) patterns were detected in the TCC (300 μg/L) experimental and control groups. The results of GO function analysis and KEGG pathway of DGE showed that aryl hydrocarbon receptor (AhR) activation and cyp-related genes (cyp1a, cyp1b1 and cyp1c) were significantly up-regulated. these affected the normal development of zebrafish embryonic heart, tissue edema, and hemorrhage. TCC exhibited strong cardiac teratogenic effects and developmental toxicity, which is partly related to AhR activation. Transcriptome-based results are helpful in precisely determining the risk of TCC exposure. The potential mechanism between TCC and AhR should be further investigated.
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http://dx.doi.org/10.1016/j.chemosphere.2021.130349DOI Listing
September 2021

tmbim4 protects against triclocarban-induced embryonic toxicity in zebrafish by regulating autophagy and apoptosis.

Environ Pollut 2021 May 5;277:116873. Epub 2021 Mar 5.

Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, PR China. Electronic address:

Triclocarban (TCC), an antibacterial agent widely used in personal care products, can affect embryonic development. However, the specific molecular mechanism of TCC-induced embryonic developmental damage remains unclear. In this study, TCC exposure was found to increase the expression of tmbim4 gene in zebrafish embryos. The tmbim4 mutant embryos are more susceptible to TCC exposure than wild-type (WT) embryos, with tmbim4 overexpression reducing TCC-induced embryonic death in the former. Exposure of tmbim4 mutant larvae to 400 μg/L TCC substantially increased apoptosis in the hindbrain and eyes. RNA-sequencing of WT and tmbim4 mutant larvae indicated that knockout of the tmbim4 gene in zebrafish affects the autophagy pathway. Abnormalities in autophagy can increase apoptosis and TCC exposure caused abnormal accumulation of autophagosomes in the hindbrain of tmbim4 mutant zebrafish embryos. Pretreatment of TCC-exposed tmbim4 mutant zebrafish embryos with autophagosome formation inhibitors, substantially reduced the mortality of embryos and apoptosis levels. These results indicate that defects in the tmbim4 gene can reduce zebrafish embryo resistance to TCC. Additionally, apoptosis induced by abnormal accumulation of autophagosomes is involved in this process.
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http://dx.doi.org/10.1016/j.envpol.2021.116873DOI Listing
May 2021

Effect of paternal age on offspring birth defects: a systematic review and meta-analysis.

Aging (Albany NY) 2020 11 20;12(24):25373-25394. Epub 2020 Nov 20.

Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Objective: This systematic review and meta-analysis was aimed at determining whether paternal age is a risk factor for offspring birth defects.

Results: A total of 38 and 11 studies were included in the systematic review and meta-analysis, respectively. Compared with reference, fathers aged 25 to 29, young fathers (< 20 years) could increase the risk of urogenital abnormalities (OR: 1.50, 95 % CI: 1.03-2.19) and chromosome disorders (OR: 1.38, 95 % CI: 1.12-1.52) in their offsprings; old fathers (≥ 40 years) could increase the risk of cardiovascular abnormalities (OR: 1.10, 95 % CI: 1.01-1.20), facial deformities (OR: 1.08, 95 % CI: 1.00-1.17), urogenital abnormalities (OR: 1.28, 95 % CI: 1.07-1.52), and chromosome disorders (OR: 1.30, 95 % CI: 1.12-1.52).

Conclusions: Our study indicated that paternal age is associated with a moderate increase in the incidence of urogenital and cardiovascular abnormalities, facial deformities, and chromosome disorders.

Methods: PubMed, Web of Science, the Cochrane Library, and Embase were searched for relevant literatures from 1960 to February 2020. The systematic review follows PRISMA guidelines. Relevant meta-analyses were performed.
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http://dx.doi.org/10.18632/aging.104141DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7803514PMC
November 2020

Catalpol ameliorates advanced glycation end product-induced dysfunction of glomerular endothelial cells via regulating nitric oxide synthesis by inducible nitric oxide synthase and endothelial nitric oxide synthase.

IUBMB Life 2019 09 12;71(9):1268-1283. Epub 2019 Mar 12.

Department of Pharmacology, School of Pharmacy, Hanlin College, Nanjing University of Chinese Medicine, Taizhou, People's Republic of China.

Catalpol (Cat.) is an iridoid glucoside extracted from the root of Rehmannia glutinosa Libosch. In this study, we investigated whether Cat. could protect the mouse glomerular endothelial cells against the deleterious effect induced by advanced glycation end products (AGEs) and explored potential mechanisms. We found that 10 μM Cat. showed a protective effect on dead cells stimulated by AGEs. Cat. significantly decreased the expression of p-NF-κBp65 and inducible nitric oxide synthase (iNOS) and increased the expression of phosphorylated-endothelial nitric oxide synthase (p-eNOS; Ser1177), PI3K, p-Akt (Thr308), and total-Akt. Moreover, Cat. restored the integrity of glomerular endothelial barrier by increasing endothelial tight gap junction protein and ameliorated the endothelial hyperpermeability induced by AGEs via modulating the nitric oxide (NO) production. Additionally, Cat. attenuated the massive release of NO induced by AGEs, inhibiting the macrophage infiltration by modulating the NO production, accompanied by the decrease in the release of monocyte chemoattractant protein-1 and intercellular cell adhesion molecule-1 in vitro. Therefore, Cat. ameliorated AGEs-induced endothelial dysfunction via inhibiting the NF-κB/iNOS pathway and activating the PI3K/Akt/eNOS pathway. © 2019 IUBMB Life, 71(9):1268-1283, 2019.
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http://dx.doi.org/10.1002/iub.2032DOI Listing
September 2019
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