Fig 2: mRNA expression of target genes CYP1A1 and NF-?B in rat lung tissues detected by reverse transcription-quantitative PCR. (A) The mRNA expression of target gene CYP1A1 in rat lung tissues: (a) Four weeks of treatment. CYP1A1 mRNA expression in rat lung tissue significantly increased with CS exposure. EGCG intervention significantly inhibited CYP1A1 mRNA overexpression. (b) Eight weeks of treatment. CYP1A1 mRNA expression was further increased in the lung tissue of rats treated with CS. EGCG intervention significantly inhibited CYP1A1 mRNA overexpression. (c) Twelve weeks of treatment. CYP1A1 mRNA expression increased in rat lung tissue following CS exposure. EGCG intervention significantly reduced cigarette-induced CYP1A1 mRNA overexpression. (d) Sixteen weeks of treatment. CYP1A1 mRNA reached its highest expression levels after 16 weeks of CS; this was significantly attenuated with EGCG treatment. (B) The mRNA expression of target gene NF-?B in rat lung tissues: (a) Four weeks of treatment. NF-?B mRNA expression in the lung tissue of rats treated with CS was significantly increased. EGCG significantly inhibited NF-?B mRNA overexpression induced by cigarette smoking. (b) Eight weeks of treatment. NF-?B mRNA expression was highest after eight weeks of CS exposure; this was significantly inhibited by EGCG intervention. (c) Twelve weeks of treatment. On the 12thweek of cigarette exposure, NF-?B mRNA levels had decreased; however, EGCG intervention still had slightly lower mRNA levels. (d) Sixteen weeks of treatment. NF-?B expression in the lung tissues of rats in the CS treatment group was not significantly different from that in the CS+EGCG treatment group. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. NF-?B, nuclear factor-?B; EGCG, epigallocatechin-3-gallate; CS, cigarette smoke; ns, no significance.

Fig 3: Protein expression of target genes CYP1A1 and NF-?B in rat lung tissues detected by western blotting. In the control group, the lung tissue of the rats revealed low expression of CYP1A1. After 4 weeks of CS, the expression of CYP1A1 protein in rat lung tissues increased. From week 8 to week 16, there was significant overexpression of CYP1A1 protein in the rat lungs exposed to CS. EGCG treatment significantly downregulated the overexpression of CYP1A1 protein in rat lung tissues induced by CS. NF-?B was weakly expressed in the lung tissue of control rats. Between weeks 4 and 12, CS increased the protein expression of NF-?B in rat lung tissue, while EGCG administration downregulated this expression. However, NF-?B overexpression then decreased until the experimental endpoint in both treatment groups. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. NF-?B, nuclear factor-?B; EGCG, epigallocatechin-3-gallate; CS, cigarette smoke.