Effects of Acupuncture on mRNA Levels of Apoptotic Factors in Perihematomal Brain Tissue During the Acute Phase of Cerebral Hemorrhage

et al. 2019

Nickel oxide nanoparticles (Nano NiO) could induce pulmonary fibrosis, however, the mechanisms are still unknown. The aim of the present study was to explore the roles of transforming growth factor‐β1 (TGF‐β1), mitogen‐activated protein kinase (MAPK) pathway and MMPs/TIMPs balance in Nano NiO‐induced pulmonary fibrosis. For that purpose, we first established Nano NiO‐induced human lung adenocarcinoma epithelial cells (A549 cells) model of collagen excessive formation through detecting the levels of hydroxyproline (Hyp) and type I collagen (Col‐I). Then the protein levels of TGF‐β1, MAPKs, and MMPs/TIMPs were assessed by Western blot. The results showed that Nano NiO resulted in the increased contents of Hyp, Col‐I, and TGF‐β1, the MAPK pathway activation and MMPs/TIMPs imbalance with a dose‐dependent manner. In addition, to investigate whether TGF‐β1 mediated MAPK signaling pathway, A549 cells were treated by 100 μg/mL Nano NiO combined with TGF‐β1, p38 MAPK, and ERK1/2 inhibitors (10 μM SB431542, 10 μM SB203580, and 10 μM U0126), respectively. We found that MAPK signal pathway was suppressed by TGF‐β1 inhibitor. Meanwhile, the increased contents of Hyp and Col‐I, and MMPs/TIMPs imbalance were alleviated by the p38 MAPK and ERK1/2 inhibitors, respectively. These findings indicated that the MAPK pathway and MMPs/TIMPs imbalance were involved in collagen excessive formation induced by Nano NiO.

Section: Methodsmentioning

confidence: 99%

TGF‐β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells

Tian

Chang

et al. 2019

“…β ‐Actin was used as the internal reference. The mRNA levels of testosterone synthetase, including StAR , CYP11A1 and 17 β ‐HSD were calculated according to the 2 −ΔΔct formula …”

Section: Methodsmentioning

confidence: 99%

Nano‐selenium attenuates nickel‐induced testosterone synthesis disturbance through inhibition of MAPK pathways in Sprague‐Dawley rats

Gan

Qiannan

et al. 2019

The aim of this study was to investigate the protective effects of Nano-Se against Ni-induced testosterone synthesis disorder in rats and determine the underlying protective mechanism. Sprague-Dawley rats were co-treated with Ni (5.0 mg/kg, i.p.) and Nano-Se (0.5, 1.0, and 2.0 mg/kg, oral gavage) for 14 days after which various endpoints were evaluated. The Ni-induced abnormal pathological changes and elevated 8-OHdG levels in the testes were attenuated by Nano-Se administration.Importantly, decreased serum testosterone levels in the Ni-treated rats were significantly restored by Nano-Se treatment, particularly at 1.0 and 2.0 mg/kg. Furthermore, the mRNA and protein levels of testosterone synthetase were increased by Nano-Se compared to the Ni group, whereas phosphorylated protein expression levels of mitogen-activated protein kinase (MAPK) pathways were suppressed by Nano-Se administration in the Ni-treated rats. Overall, the results suggest that Nano-Se may ameliorate the Ni-induced testosterone synthesis disturbance via the inhibition of ERK1/2, p38, and JNK MAPK pathways.

“…RT‐qPCR was performed with Bestar SYBR Green qPCR Mastermix kits (DBI Bioscience, Germany) in an IQ5 Multicolor Real‐Time PCR Detection System (Bio‐Rad) 20 . The mRNA expression levels were measured by relative quantitative 2 −ΔΔct method 21 …”

Section: Methodsmentioning

confidence: 99%

Nano nickel oxide promotes epithelial‐mesenchymal transition through transforming growth factor β1/smads signaling pathway in A549 cells

Chang

Tian

et al. 2020

Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation in A549 cells, which mechanism was related with the increasing transforming growth factor β1 (TGF‐β1) secretion. However, it remains unclear understanding the role of TGF‐β1 in collagen excessive formation. Here, we found nano NiO could directly promote epithelial‐mesenchymal transition (EMT) via the TGF‐β1/Smads pathway in A549 cells. First, cytotoxicity induced by nano NiO has a dose‐ and time‐dependent manner according to methylthiaozol tetrazolium assay. Second, nano NiO led to the increased contents of type I collagen (Col‐I), TGF‐β1, p‐Smad2, p‐Smad3, alpha‐smooth muscle actin (α‐SMA), vimentin, and fibronectin, indicating Smads pathway activation and EMT occurence. Third, to verify whether TGF‐β1 activated Smads signaling pathway and EMT occurence, A549 cells were exposed to nano NiO and TGF‐β1 inhibitors (10 μM SB431542). The results showed that TGF‐β1 inhibitors alleviated the nano NiO‐induced cytotoxicity and Col‐I excessive formation. Meanwhile, TGF‐β1 inhibitors reversed the proteins expression trends of Col‐I, p‐Smad2, p‐Smad3, α‐SMA, vimentin, fibronectin, and E‐cadherin. These observations suggested that EMT occurrence via TGF‐β1/Smads pathway might play an important role in the collagen excessive formation induced by nano NiO in A549 cells.