Baicalein inhibits cell proliferation and enhances apoptosis in human A549 cells and benzo(a)pyrene‐induced pulmonary carcinogenesis in mice

Abstract

Our current study is done to explore the possible mechanisms to elaborate on the growth inhibitory effect of baicalein (BE) in human lung carcinoma. Initially, BE (25 and 50 µM) treatment for 24 h, suppressed the viability and inhibited population growth in A549 cells. BE upholds the production of reactive oxygen species (ROS) with concomitant replenishment of glutathione, catalase, and glutathione peroxidase activity. The expression level of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 markedly increased after BE treatment will intimidate A549 cells proliferation by the ROS-independent pathway via the antioxidant pathway. In vivo investigations were carried out on BE (12 mg/kg, oral) in benzo(a)pyrene (B(a)P; 50 mg/kg, oral) induced lung carcinogenesis in mice. BE induces caspase-dependent apoptosis by increasing the levels of cytosolic cytochrome c accompanied by upregulating the outflow of p53, Bax, and caspase-3 with a concomitant abatement in the outflow of Bcl-2 in both in vitro and in vivo. In the murine model, BE treatment hindered the countenance of proliferation-related proteins (argyrophilic nucleolar organizing regions and proliferating cell nuclear antigen). Additionally, appraisal of the cell nucleus by transmission electron microscopic assessment uncovered that BE treatment adequately counteracts B(a)P-induced lung cancer cell survival. During the transition of the G 0 /G 1 phase, BE is arrested in the cell cycle process. This might be the cause of a substantial increase in the appearance of p21 Cip1 with concomitant downregulating the expressions of CDK4, cyclin D, and cyclin E both in vitro and in vivo. Our results conclude that BE treatment induced apoptosis and repressed proliferation both in vitro and in vivo of human lung carcinoma.

Peroxiredoxin 5 protects HepG2 cells from ethyl β-carboline-3-carboxylate-induced cell death via ROS-dependent MAPK signalling pathways

“…In the ongoing process of drug development, chemotherapy medications have gradually become the first choice of treatment. These chemotherapeutic drugs exhibit anti-cancer effects such as regulating intracellular ROS levels by generating DNA damage in cancer cells [20], initiating cell cycle organization [21], and creating mitochondrial dysfunction [22]. ROS is the main cause of oxidative stress, and the basal level of redox processes in cancer cells is relatively high [23].…”