Background The intestinal epithelium performs essential physiological functions,such as nutrient absorption,and acts as a barrier to prevent the entry of harmful substances.Mycotoxins are prevalent contaminants found ...Background The intestinal epithelium performs essential physiological functions,such as nutrient absorption,and acts as a barrier to prevent the entry of harmful substances.Mycotoxins are prevalent contaminants found in ani-mal feed that exert harmful effects on the health of livestock.Zearalenone(ZEA)is produced by the Fusarium genus and induces gastrointestinal dysfunction and disrupts the health and immune system of animals.Here,we evaluated the molecular mechanisms that regulate the effects of ZEA on the porcine intestinal epithelium.Results Treatment of IPEC-J2 cells with ZEA decreased the expression of E-cadherin and increased the expression of Snai1 and Vimentin,which induced Snail1-mediated epithelial-to-mesenchymal transition(EMT).In addition,ZEA induces Snail-mediated EMT through the activation of TGF-βsignaling.The treatment of IPEC-J2 cells with atractyle-nolideⅢ,which were exposed to ZEA,alleviated EMT.Conclusions Our findings provide insights into the molecular mechanisms of ZEA toxicity in porcine intestinal epi-thelial cells and ways to mitigate it.展开更多
Objective:To investigate the effect nano-sustained CO-releasing molecules on cyclosporin-A(CsA)-induced nephrotoxicity by inhibiting the NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.Methods:3×105 cel...Objective:To investigate the effect nano-sustained CO-releasing molecules on cyclosporin-A(CsA)-induced nephrotoxicity by inhibiting the NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.Methods:3×105 cell/mL human renal tubular epithelial cells(HK-2)and mouse primary cultured renal tubular epithelial cells(RTECs)were cultured under an inverted microscope and incubated with 10%DMEM and 0.25%β2M in NaCl solution for 3 h.HK-2 and RTECs were divided into 5 complex numbers.MTT assay was used to detect the relative proliferation level of one of the HK-2 cells and calculate the multiplication ratio.Results:The nano-sustained CO-releasing molecules CS-CO had a strong protective effect on the kidney.HK-2 and RTECs cells were treated with siRNA,inhibitors,and NLRP3 knockout mice,and the changes in cell activity and expression of intracellular inflammatory factors were studied.The expression of TGF-β1/Smad signaling pathway related proteins in HK-2 and RTECs was detected by ELISA,western blot,immunofluorescence,and other techniques.Conclusion:SMA/CORM2 alleviates CsA-induced renal fibrosis by inhibiting NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.展开更多
Objective: In women with pelvic organ prolapse (POP), decreased expression of transforming growth factor-beta 1 (TGF-β1) has been shown in POP tissues. However, no studies have evaluated plasma TGF-β1 levels in pati...Objective: In women with pelvic organ prolapse (POP), decreased expression of transforming growth factor-beta 1 (TGF-β1) has been shown in POP tissues. However, no studies have evaluated plasma TGF-β1 levels in patients with POP, so it is unknown whether they are also changed or not. Therefore, we compared plasma TGF-β1 levels in women with and without POP. Methods: Participants were 49 women with POP and 23 healthy control women. All participants were postmenopausal. We measured plasma TGF-β1 and compared data between patients with POP and controls, and between patients with uterine prolapse (UP, n = 19) and those with a cystocele (CC, n = 30). In addition, in patients, we assessed the POP quantification system (POP-Q) stage. Results: Plasma TGF-β1 levels were significantly lower in patients than in healthy controls. POP-Q stage was not significantly different between the UP and CC subgroups, but POP-Q stage IV was diagnosed in 63% of patients with UP and 7% of those with CC. Plasma TGF-β1 levels were significantly lower in the CC subgroup than in the UP subgroup. Conclusion: Plasma TGF-β1 is decreased in POP. It remains unclear whether the lower levels indicate a reduction in systemic TGF-β1 activity, but they can be assumed to reflect reduced TGF-β1 expression in POP tissues.展开更多
基金supported by the Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(2022R1I1A3070740)。
文摘Background The intestinal epithelium performs essential physiological functions,such as nutrient absorption,and acts as a barrier to prevent the entry of harmful substances.Mycotoxins are prevalent contaminants found in ani-mal feed that exert harmful effects on the health of livestock.Zearalenone(ZEA)is produced by the Fusarium genus and induces gastrointestinal dysfunction and disrupts the health and immune system of animals.Here,we evaluated the molecular mechanisms that regulate the effects of ZEA on the porcine intestinal epithelium.Results Treatment of IPEC-J2 cells with ZEA decreased the expression of E-cadherin and increased the expression of Snai1 and Vimentin,which induced Snail1-mediated epithelial-to-mesenchymal transition(EMT).In addition,ZEA induces Snail-mediated EMT through the activation of TGF-βsignaling.The treatment of IPEC-J2 cells with atractyle-nolideⅢ,which were exposed to ZEA,alleviated EMT.Conclusions Our findings provide insights into the molecular mechanisms of ZEA toxicity in porcine intestinal epi-thelial cells and ways to mitigate it.
基金Health Commission of Hebei Province Chuanxiong:Extract Improves Inflammatory Response in Rats with Pyelonephritis through IL-6/STAT3 Signaling Pathway(Project number:20231486)。
文摘Objective:To investigate the effect nano-sustained CO-releasing molecules on cyclosporin-A(CsA)-induced nephrotoxicity by inhibiting the NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.Methods:3×105 cell/mL human renal tubular epithelial cells(HK-2)and mouse primary cultured renal tubular epithelial cells(RTECs)were cultured under an inverted microscope and incubated with 10%DMEM and 0.25%β2M in NaCl solution for 3 h.HK-2 and RTECs were divided into 5 complex numbers.MTT assay was used to detect the relative proliferation level of one of the HK-2 cells and calculate the multiplication ratio.Results:The nano-sustained CO-releasing molecules CS-CO had a strong protective effect on the kidney.HK-2 and RTECs cells were treated with siRNA,inhibitors,and NLRP3 knockout mice,and the changes in cell activity and expression of intracellular inflammatory factors were studied.The expression of TGF-β1/Smad signaling pathway related proteins in HK-2 and RTECs was detected by ELISA,western blot,immunofluorescence,and other techniques.Conclusion:SMA/CORM2 alleviates CsA-induced renal fibrosis by inhibiting NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.
文摘Objective: In women with pelvic organ prolapse (POP), decreased expression of transforming growth factor-beta 1 (TGF-β1) has been shown in POP tissues. However, no studies have evaluated plasma TGF-β1 levels in patients with POP, so it is unknown whether they are also changed or not. Therefore, we compared plasma TGF-β1 levels in women with and without POP. Methods: Participants were 49 women with POP and 23 healthy control women. All participants were postmenopausal. We measured plasma TGF-β1 and compared data between patients with POP and controls, and between patients with uterine prolapse (UP, n = 19) and those with a cystocele (CC, n = 30). In addition, in patients, we assessed the POP quantification system (POP-Q) stage. Results: Plasma TGF-β1 levels were significantly lower in patients than in healthy controls. POP-Q stage was not significantly different between the UP and CC subgroups, but POP-Q stage IV was diagnosed in 63% of patients with UP and 7% of those with CC. Plasma TGF-β1 levels were significantly lower in the CC subgroup than in the UP subgroup. Conclusion: Plasma TGF-β1 is decreased in POP. It remains unclear whether the lower levels indicate a reduction in systemic TGF-β1 activity, but they can be assumed to reflect reduced TGF-β1 expression in POP tissues.
