AIM: To investigate the protective role of magnolol in the treatment of acute lung injury induced by acute necrotizing pancreatitis (ANP) in rats. METHODS: Fifty-six Sprague-Dawley rats were divided into sham operation group, ANP group, and magnolol treatment group. ANP model was induced by retrograde infusion of 50 g/L so- dium taurocholate into the biliopancreatic duct of rats. The mRNA expression of nuclear factor- kappa B (NF-kB), tumor necrosis factor-alpha (TNF-a), and interleukin-10 (IL-10) in lung tis- sue were assayed using fluorescence quantita- tive polymerase chain reaction (FQ-PCR) at 6, 12, and 24 h. Meanwhile, the activity of serum amylase (Amy) was also determined, and the pathological changes of the pancreas and lung were observed. RESULTS: In comparison with those in shamoperation group, the expression of NF-kB, TNF-a, and IL-10 mRNA and the activity of se- rum Amy in ANP group were increased signifi- cantly (P < 0.01), and the expression of NF-kB, TNF-a mRNA and the activity of Amy reached the peak at 12 h. The expression of IL-10 mRNA increased gradually at 6, 12, and 24 h (0.20 ± 0.05, 0.27 ± 0.07, 0.45 ± 0.20, respectively). Magnolol treatment resulted in lower expression of NF- kB, TNF-a mRNA and serum Amy levels (1.30 ± 0.14 vs 1.84 ± 0.56, 0.41 ± 0.19 vs 0.72 ± 0.36, both P < 0.05; 104 576 ± 24 886 nkat/L vs 188 621 ± 23 747 nkat/L, P < 0.01, respectively, at 12 h), but didn’t alter the expression of IL-10 mRNA (P > 0.05) as compared with that in ANP group. Magnolol treatment relieved the pathological changes markedly in the lung tissues but not in the pancreatic tissues. CONCLUSION: Magnolol can decrease the ex- pression of the proinflammatory factors such as NF-kB and TNF-a and relieve the acute lung injury induced by acute necrotizing pancreatitis in rats.