GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway
Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhan...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Yue-Ying [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Physical activity temporal trends among children and adolescents - Booth, Verity M. ELSEVIER, 2015, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:118 ; year:2018 ; pages:395-402 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.rvsc.2018.04.004 |
|---|
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ELV043224350 |
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| 245 | 1 | 0 | |a GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway |
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| 520 | |a Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. | ||
| 520 | |a Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. | ||
| 700 | 1 | |a Sun, Shi-Ping |4 oth | |
| 700 | 1 | |a Zhu, He-Shui |4 oth | |
| 700 | 1 | |a Jiao, Xian-Qin |4 oth | |
| 700 | 1 | |a Zhong, Kai |4 oth | |
| 700 | 1 | |a Guo, Yu-Jie |4 oth | |
| 700 | 1 | |a Zha, Guang-Ming |4 oth | |
| 700 | 1 | |a Han, Li-Qiang |4 oth | |
| 700 | 1 | |a Yang, Guo-Yu |4 oth | |
| 700 | 1 | |a Li, He-Ping |4 oth | |
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10.1016/j.rvsc.2018.04.004 doi GBV00000000000579.pica (DE-627)ELV043224350 (ELSEVIER)S0034-5288(18)30029-8 DE-627 ger DE-627 rakwb eng 610 VZ 796 VZ 670 VZ 51.60 bkl 58.45 bkl Wang, Yue-Ying verfasserin aut GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Sun, Shi-Ping oth Zhu, He-Shui oth Jiao, Xian-Qin oth Zhong, Kai oth Guo, Yu-Jie oth Zha, Guang-Ming oth Han, Li-Qiang oth Yang, Guo-Yu oth Li, He-Ping oth Enthalten in Elsevier Booth, Verity M. ELSEVIER Physical activity temporal trends among children and adolescents 2015 Amsterdam [u.a.] (DE-627)ELV012775517 volume:118 year:2018 pages:395-402 extent:8 https://doi.org/10.1016/j.rvsc.2018.04.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_24 GBV_ILN_60 GBV_ILN_181 GBV_ILN_227 GBV_ILN_352 GBV_ILN_2084 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 118 2018 395-402 8 |
| spelling |
10.1016/j.rvsc.2018.04.004 doi GBV00000000000579.pica (DE-627)ELV043224350 (ELSEVIER)S0034-5288(18)30029-8 DE-627 ger DE-627 rakwb eng 610 VZ 796 VZ 670 VZ 51.60 bkl 58.45 bkl Wang, Yue-Ying verfasserin aut GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Sun, Shi-Ping oth Zhu, He-Shui oth Jiao, Xian-Qin oth Zhong, Kai oth Guo, Yu-Jie oth Zha, Guang-Ming oth Han, Li-Qiang oth Yang, Guo-Yu oth Li, He-Ping oth Enthalten in Elsevier Booth, Verity M. ELSEVIER Physical activity temporal trends among children and adolescents 2015 Amsterdam [u.a.] (DE-627)ELV012775517 volume:118 year:2018 pages:395-402 extent:8 https://doi.org/10.1016/j.rvsc.2018.04.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_24 GBV_ILN_60 GBV_ILN_181 GBV_ILN_227 GBV_ILN_352 GBV_ILN_2084 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 118 2018 395-402 8 |
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10.1016/j.rvsc.2018.04.004 doi GBV00000000000579.pica (DE-627)ELV043224350 (ELSEVIER)S0034-5288(18)30029-8 DE-627 ger DE-627 rakwb eng 610 VZ 796 VZ 670 VZ 51.60 bkl 58.45 bkl Wang, Yue-Ying verfasserin aut GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Sun, Shi-Ping oth Zhu, He-Shui oth Jiao, Xian-Qin oth Zhong, Kai oth Guo, Yu-Jie oth Zha, Guang-Ming oth Han, Li-Qiang oth Yang, Guo-Yu oth Li, He-Ping oth Enthalten in Elsevier Booth, Verity M. ELSEVIER Physical activity temporal trends among children and adolescents 2015 Amsterdam [u.a.] (DE-627)ELV012775517 volume:118 year:2018 pages:395-402 extent:8 https://doi.org/10.1016/j.rvsc.2018.04.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_24 GBV_ILN_60 GBV_ILN_181 GBV_ILN_227 GBV_ILN_352 GBV_ILN_2084 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 118 2018 395-402 8 |
| allfieldsGer |
10.1016/j.rvsc.2018.04.004 doi GBV00000000000579.pica (DE-627)ELV043224350 (ELSEVIER)S0034-5288(18)30029-8 DE-627 ger DE-627 rakwb eng 610 VZ 796 VZ 670 VZ 51.60 bkl 58.45 bkl Wang, Yue-Ying verfasserin aut GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Sun, Shi-Ping oth Zhu, He-Shui oth Jiao, Xian-Qin oth Zhong, Kai oth Guo, Yu-Jie oth Zha, Guang-Ming oth Han, Li-Qiang oth Yang, Guo-Yu oth Li, He-Ping oth Enthalten in Elsevier Booth, Verity M. ELSEVIER Physical activity temporal trends among children and adolescents 2015 Amsterdam [u.a.] (DE-627)ELV012775517 volume:118 year:2018 pages:395-402 extent:8 https://doi.org/10.1016/j.rvsc.2018.04.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_24 GBV_ILN_60 GBV_ILN_181 GBV_ILN_227 GBV_ILN_352 GBV_ILN_2084 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 118 2018 395-402 8 |
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10.1016/j.rvsc.2018.04.004 doi GBV00000000000579.pica (DE-627)ELV043224350 (ELSEVIER)S0034-5288(18)30029-8 DE-627 ger DE-627 rakwb eng 610 VZ 796 VZ 670 VZ 51.60 bkl 58.45 bkl Wang, Yue-Ying verfasserin aut GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. Sun, Shi-Ping oth Zhu, He-Shui oth Jiao, Xian-Qin oth Zhong, Kai oth Guo, Yu-Jie oth Zha, Guang-Ming oth Han, Li-Qiang oth Yang, Guo-Yu oth Li, He-Ping oth Enthalten in Elsevier Booth, Verity M. ELSEVIER Physical activity temporal trends among children and adolescents 2015 Amsterdam [u.a.] (DE-627)ELV012775517 volume:118 year:2018 pages:395-402 extent:8 https://doi.org/10.1016/j.rvsc.2018.04.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_24 GBV_ILN_60 GBV_ILN_181 GBV_ILN_227 GBV_ILN_352 GBV_ILN_2084 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 118 2018 395-402 8 |
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gaba regulates the proliferation and apoptosis of mac-t cells through the lps-induced tlr4 signaling pathway |
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GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway |
| abstract |
Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. |
| abstractGer |
Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. |
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Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway. |
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GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway |
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