Publications by authors named "Yingfang Guo"

8 Publications

  • Page 1 of 1

Reduced expression of MiR-125a-5p aggravates LPS-induced experimental acute kidney injury pathology by targeting TRAF6.

Life Sci 2021 May 25:119657. Epub 2021 May 25.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China. Electronic address:

Aims: Patients with acute kidney injury (AKI) have higher mortality, and sepsis is among its main causes. MicroRNAs (miRNAs) are essential for regulating kidney function and could have curative potential. This study explored the possibility to treat AKI with miR-125a-5p and reveal the possible mechanism.

Materials And Methods: LPS-induced mouse model and LPS-induced RAW264.7 cell model of AKI were established and treated with miR-125a-5p mimics or inhibitors. Serum creatinine and blood urea were measured to evaluate kidney function. The pathological changes of kidney tissues were detected by H&E and PAS staining technique, and the infiltration of macrophages were observed by immunohistochemistry. RAW264.7 cell viability, TRAF6 and cytokines expressions under LPS stimulation were measured. The role and therapeutic potential of miR-125a-5p were verified in vivo and in vitro after given miR-125a-5p mimics or inhibitors.

Key Findings: LPS-induced mice had increasing serum creatinine and urea, and evident pathological changes, including severe tubular dilatation and macrophages infiltration. TRAF6 expression in the kidney was significantly higher, while miR-125a-5p expression was suppressed. MiR-125a-5p targeted TRAF6, and its overexpression deactivated NF-κB signaling pathway, reducing downstream TNF-α, IL-1β and IL-6 expressions. MiR-125a-5p mimics rescued LPS-induced kidney damage and suppressed pro-inflammatory cytokines expression through inhibiting TRAF6/NF-κB axis.

Significance: We highlighted that miR-125a-5p could inhibit LPS-induced acute inflammation in the kidney through targeting TRAF6/NF-κB axis. These results might contribute to the development of molecular therapy in AKI.
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http://dx.doi.org/10.1016/j.lfs.2021.119657DOI Listing
May 2021

MicroRNA-211 regulates the expression of TAB1 and inhibits the NF-κB signaling pathway in lipopolysaccharide-induced endometritis.

Int Immunopharmacol 2021 May 10;96:107668. Epub 2021 May 10.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China. Electronic address:

Endometritis is a common postpartum inflammatory disease that endangers the reproductive health of humans and animals. Emerging evidence shows that microRNA is a new type of therapeutic molecule that plays a vital role in many diseases; however, its mechanism of action in lipopolysaccharide (LPS)-induced endometritis is still unclear. This study aims to investigate the regulatory role of miR-211 in the innate immune response involved in endometritis, and to evaluate its potential therapeutic value. Here, we found that the expression of miR-211 in bovine endometrial epithelial cells (bEECs) stimulated by lipopolysaccharide (LPS) was significantly reduced. Importantly, overexpression of miR-211 can significantly reduce the production of pro-inflammatory cytokines (IL-1β , IL-6 and TNF-α). In addition, we proved that TAB1 is the target gene of miR-211. MiR-211 inhibits TAB1 protein expression by binding to the 3'-UTR of TAB1 mRNA. Subsequently, we verified that the overexpression of miR-211 inhibited the activation of NF-κB p65 by targeting the TAB1-mediated pathway. Therefore, miR-211 has anti-inflammatory effects and mediates the negative regulation of the NF-κB signaling pathway in LPS-induced endometritis by targeting TAB1.
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http://dx.doi.org/10.1016/j.intimp.2021.107668DOI Listing
May 2021

6-Gingerol exerts anti-inflammatory effects and protective properties on LTA-induced mastitis.

Phytomedicine 2020 May 26;76:153248. Epub 2020 May 26.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China. Electronic address:

Background: Mastitis has a severe impact on human health and breastfeeding. Gram-positive bacteria are one of the most common pathogens, of which lipoteichoic acid (LTA) serves as the main pathogenic factor. Bio-active extractions from herbs is regarded as an alternative method to antibiotics. 6-Gingerol is used for the treatment of tumors and inhibition of inflammation in liver and gallbladder.

Purpose: To determine whether 6-gingerol can be used as a therapeutic medicine for mastitis.

Results: In this article, we used mice as the animal model and RAW264.7/PMECs as cell models. Western blot was for detecting the expression of proteins in NF-κB/MAPK signaling pathways and MMPs/TIMPs. MPO was for the detection of the amount of immune cells. H&E, immunohistochemistry and immunofluorescence were used for locating and detecting the expression of proteins. The detection of inflammatory cytokines was conducted by ELISA and RT-qPCR. We found that the NF-κB/MAPK signaling pathways, formation of ECM, production of inflammatory cytokines and injury to mammary gland cells were attenuated both in vivo and in vitro when 6-gingerol was administered.

Conclusion: We discovered the function and efficacy of 6-gingerol as a therapeutic compound in LTA-induced mastitis and its probable mechanism of action.
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http://dx.doi.org/10.1016/j.phymed.2020.153248DOI Listing
May 2020

Gas6 negatively regulates the Staphylococcus aureus-induced inflammatory response via TLR signaling in the mouse mammary gland.

J Cell Physiol 2020 10 13;235(10):7081-7093. Epub 2020 Feb 13.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, People's Republic of China.

Staphylococcus aureus (S. aureus)-induced mastitis is the most frequent, pathogenic, and prevalent infection of the mammary gland. The ligand growth arrest-specific 6 (Gas6) is a secretory protein that binds to and activates Tyro3, Axl, and MerTK receptors. This study explored the role of Gas6 in S. aureus-induced mastitis. Our results revealed that TLR receptors initiate the innate immune response in mammary gland tissues and epithelial cells and that introducing S. aureus activates TLR2 and TLR6 to drive multiple intracellular mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) pathways. Moreover, S. aureus also induces Gas6, which then activates the TAM receptor kinase pathway, which is related to the inhibition of TLR2- and TLR6-mediated inflammatory pathways through SOCS1 and SOCS3 induction. Gas6 absence alone was found to be involved in the downregulation of TAM receptor-mediated anti-inflammatory effects by inducing significantly prominent expression of TRAF6 and low protein and messenger RNA expression of SOCS1 and SOCS3. S. aureus-induced MAPK and NF-ĸB p65 phosphorylation were also dependent on Gas6, which negatively regulated the production of Pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in S. aureus-treated mammary tissues and mammary epithelial cells. Our in vivo and in vitro study uncovered the Gas6-mediated negative feedback mechanism, which inhibits TLR2- and TLR6-mediated MAPK and NF-ĸB signaling by activating TAM receptor kinase (MerTK, Axl, and Tyro3) through the induction of SOCS1/SOCS3 proteins.
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http://dx.doi.org/10.1002/jcp.29604DOI Listing
October 2020

Selenium Attenuates Staphylococcus aureus Mastitis in Mice by Inhibiting the Activation of the NALP3 Inflammasome and NF-κB/MAPK Pathway.

Biol Trace Elem Res 2019 Sep 7;191(1):159-166. Epub 2018 Dec 7.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China.

Mastitis is one of the most important diseases affecting the dairy industry in the world, and it also poses a great threat to human food safety. In this study, we explored whether selenium can inhibit the activation of the NALP3 inflammasome and NF-κB/MAPK pathway to achieve anti-inflammatory effects. Sixty BALB/c female mice were randomly divided into three groups according to diets of different selenium concentrations (high, normal, and low). After 90 days, mice fed the same selenium concentration were randomly divided into two smaller groups, one of which was inoculated with Staphylococcus aureus and the other injected with saline as a control. Through histopathologic examination staining, western blot, qPCR, and ELISA, the results showed that with increasing selenium concentrations, the expression levels of IL-1β, TNF-α, NALP3, caspase-1, and ASC were decreased in mouse mammary tissue. Therefore, this study revealed that selenium can attenuate S. aureus mastitis by inhibiting the activation of the NALP3 inflammasome and NF-κB/MAPK pathway.
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http://dx.doi.org/10.1007/s12011-018-1591-8DOI Listing
September 2019

Selenium suppresses inflammation by inducing microRNA-146a in -infected mouse mastitis model.

Oncotarget 2017 Dec 8;8(67):110949-110964. Epub 2017 Sep 8.

College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.

We studied the effects of selenium (Se) on the inflammatory response in ()-infected mastitis-model mice and mammary epithelial cells. In infected mice, Se elicited a dose-dependent decrease in mammary gland pathology that included inflammatory cell infiltration, disorganized acinar structure and mammary cell necrosis. Se decreased inflammation by increasing miR-146a and decreasing TLR2/6 as well as NF-κB and MAPK signaling pathways in mammary tissue from infected mice and mammary epithelial cells. A miR-146a inhibitor suppressed the anti-inflammatory effects of Se in infected mammary epithelial cells. Se, miR-146a and TLR2 were associated in determining the inflammatory response in mouse with infection-induced mastitis. Thus, Se inhibits pro-inflammatory responses in mammary tissues from -infected mice by inducing miR-146a.
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http://dx.doi.org/10.18632/oncotarget.20740DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762297PMC
December 2017

IFN- Displays Anti-Inflammatory Effects on Endometritis via Inhibiting the Activation of the NF-B and MAPK Pathways in Mice.

Biomed Res Int 2017 26;2017:2350482. Epub 2017 Feb 26.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.

The aim of the present study was to determine the anti-inflammatory effect of IFN- on endometritis using a mouse model of -induced endometritis and to elucidate the mechanism of action underlying these effects. In the present study, the effect of IFN- on growth was monitored by turbidimeter at 600 nm. IFN- did not affect growth. The histopathological changes indicated that IFN- had a protective effect on uterus tissues with infection. The ELISA and qPCR results showed the production of the proinflammatory cytokines TNF-, IL-1, and IL-6 was decreased with IFN- treatment. In contrast, the level of the anti-inflammatory cytokine IL-10 was increased. We further studied the signaling pathway associated with these observations, and the qPCR results showed that the expression of TLR2 was repressed by IFN-. Furthermore, the western blotting results showed the phosphorylation of IB, NF-B p65, and MAPKs (p38, JNK, and ERK) was inhibited by IFN- treatment. The results suggested that IFN- may be a potential drug for the treatment of uterine infection due to or other infectious inflammatory diseases.
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http://dx.doi.org/10.1155/2017/2350482DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346370PMC
April 2017

Protective Action of Se-Supplement Against Acute Alcoholism Is Regulated by Selenoprotein P (SelP) in the Liver.

Biol Trace Elem Res 2017 Feb 22;175(2):375-387. Epub 2016 Jun 22.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China.

Acute alcoholism is a major cause of cirrhosis and liver failure around the world. Selenium (Se) is an essential micronutrient promoting liver health in humans and animals. Selenoprotein P (SelP) is a glycoprotein secreted within the liver, which interacts with cytokines and the growth factor pathway to provide protection for hepatic cells. The present study was conducted to confirm the effect and mechanism of Se and SelP action in livers affected by acute alcoholism. In this study, a mouse model of acute alcoholism, as well as a hepatocyte model, was successfully established. The Se content of the liver was detected by atomic fluorescence spectrophotometry. The expression of messenger RNA (mRNA) was analyzed by quantitative polymerase chain reaction (qPCR). The protein expression of inflammatory factors was detected by ELISA. The other proteins were analyzed by western blotting. The results showed that pathological damage to the liver was gradually weakened by Se-supplementation, which was evaluated by hematoxylin and eosin (H&E) and TUNEL staining. Se-supplementation inhibited expression of pro-inflammatory factors TNF-α and IL-1β and promoted production of anti-inflammatory cytokine IL-10 in the liver with acute alcoholism. Se-supplementation also prevented the apoptosis of hepatocytes by suppressing the cleavage of caspases-9, 3, 6, 7, and poly(ADP-ribose) polymerase (PARP). Through correlational analysis, it was determined that the effects of Se-supplement were closely related to SelP expression, inflammatory cytokines, and apoptosis molecule production. The sienna of SelP further confirmed the protective action of Se-supplementation on the liver and that the mechanism of SelP involves the regulation of inflammatory cytokines and apoptosis molecules in acute alcoholism. These findings provide information regarding a new potential target for the treatment of acute alcoholism.
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http://dx.doi.org/10.1007/s12011-016-0780-6DOI Listing
February 2017