Nickel(II) oxide

Nickel(II) oxide (12.5, 25, 50, 100, 200 μg/mL; 24 h) reduced A549 cell viability in a dose-dependent manner and increased lactate dehydrogenase (LDH) activity in the culture medium, with cell viability maintained at 60%-80% at concentrations of 25, 50, and 100 μg/mL^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently increased hydroxyproline (Hyp) content and type I collagen (Col-I) protein expression in A549 cell culture medium, with significantly increased Hyp content in the 100 μg/mL group and upregulated Col-I expression in the 50 and 100 μg/mL groups^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently upregulated TGF-β1 protein expression in A549 cells, activating the p38 MAPK and ERK1/2 pathways, with increased gene and phosphorylated protein levels while total protein levels remained unchanged^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) induced MMPs/TIMPs imbalance in A549 cells, with significantly increased MMP-9 gene and protein levels in the 50 and 100 μg/mL groups, dose-dependent upregulation of TIMP-1 and TIMP-2, and increased MMP-2 protein expression only in the 100 μg/mL group^[1].
Nickel(II) oxide (100 μg/mL; pre-treatment with inhibitor for 1 hour followed by 24 h treatment) combined with 10 μM TGF-β1 inhibitor SB431542 (HY-10431) downregulated p-p38 MAPK and p-ERK1/2 levels in A549 cells and increased cell viability^[1].
Nickel(II) oxide (100 μg/mL; pre-treatment with inhibitor for 1 hour followed by 24 h treatment) in combination with 10 μM p38 inhibitor SB203580 (HY-10256) or ERK1/2 inhibitor U0126 (HY-12031A) reduced the protein levels of Col-I, MMP-2, MMP-9, TIMP-1, and TIMP-2^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently downregulated lncRNA MEG3 expression in A549 cells, with significant effects at 50 and 100 μg/mL, and simultaneously activated the PI3K/AKT pathway (increased p-PI3K, p-AKT, and p-mTOR)^[2].

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