Fig 2: miR-125b suppresses NF-κB activation through CK2 in LPS-treated MH7A cells. MH7A cells were transfected with miR-125b mimics or cotransfected with miR-125b and pcDNA-IkB-α and then treated with LPS or PDTC. (a) The protein level of p-p65 and p-IkB-α was evaluated via western blot. (b) The cytokine protein levels including TNF-α, IL-1β, and IL-6 in the cellular supernatant were measured by using ELISA assay. N = 3, ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001.

Fig 3: HQT ameliorates LPS-induced inflammation through upregulating miR-125b to suppress NF-?B-induced inflammation by targeting CK2. (a) MH7A cells were treated with different concentrations of HQT such as 0, 0.1, 1, 10, and 100 mg/mL for 24 h; cell viability was evaluated via the CCK-8 assay. (b–e) MH7A cells were transfected with miR-125b mimics or miR-125b inhibitor and then treated with LPS and PDTC. (b) The mRNA expression of miR-125b, pre-miR-125b, and pri-miR-125b was evaluated via qRT-PCR. (c) The protein level of p-p65 and p-IkB-a was evaluated via western blot. (d) Human CK2 concentration in the cultured supernatant was measured by using an ELISA assay. (e) The cytokine protein levels including TNF-a, IL-1ß, and IL-6 in the cellular supernatant were measured by using an ELISA assay. N = 3, *p < 0.05, **p < 0.01, and ***p < 0.001.