Regulatory effect of extract of Lindera aggregata on NF-κB pathway in lung tissues of mice with acute lung injury

XU Zongjie; FAN Lu; LU Mingfeng

doi:10.3969/j.issn.1002-266X.2025.12.010

Abstract：Objective To observe the regulatory effect of the extract of Lindera aggregata on the nuclear factor-κB(NF-κB)pathway in lung tissues of mice with acute lung injury(ALI),and to explore its underlying mechanism.Meth-ods Thirty-two C57BL/6J mice were randomly divided into four groups:the normal group,the model group,the Lindera aggregata extract group,and the dexamethasone group,with 8 mice in each group.The model group,Lindera aggregata ex-tract group,and dexamethasone group were intratracheally instilled with 5 mg/kg LPS to establish the ALI models,while the normal group received an equal volume of phosphate-buffered saline.Six hours after the intratracheal instillation,the Lindera aggregata extract group was administered the extract at 5 g/(kg·d)by gavage for 5 consecutive days,and the dexa-methasone group received dexamethasone at 7.2 g/(kg·d)via intraperitoneal injection for 5 consecutive days.The normal group and the model group were given an equal volume of 0.9%sodium chloride solution by gavage for 5 consecutive days.Twenty-four hours after the last administration,the mice were anesthetized,and blood samples were collected via cardiac puncture.Bronchoalveolar lavage fluid(BALF)and lung tissues were harvested.The lung edema parameter,wet/dry(W/D)weight ratio,was calculated,and pathological changes in lung tissue were observed.The levels of interleukin-1β(IL-1β)and IL-6 were measured by ELISA.The positive expression rate of the M1 macrophage polarization marker CD86 in BALF was detected by flow cytometry.The expression levels of key proteins in the NF-κB signaling pathway,phosphorylat-ed p65(p-p65)and phosphorylated IκB(p-IκB),were determined by Western blotting.Results Compared with the normal group,the model group showed severe destruction of the alveolar structure,increased W/D ratio,elevated levels of IL-1β and IL-6 in serum and BALF,increased CD86 positive expression rate in BALF macrophages,and up-regulated ex-pression of p-p65 and p-IκB in lung tissues(all P<0.01).Compared with the model group,both the Lindera aggregata ex-tract group and the dexamethasone group exhibited alleviated alveolar structural damage,decreased W/D ratio,reduced levels of IL-1β and IL-6 in serum and BALF,declined CD86 expression rate in BALF,and down-regulated expression of p-p65 and p-IκB in lung tissues(all P<0.01).No statistically significant differences were observed between the Lindera ag-gregata extract group and the dexamethasone group in terms of serum IL-6 levels,BALF IL-1β levels,CD86 positive ex-pression rate in BALF macrophages,the expression of p-p65 or the expression of p-IκB in the lung tissues(all P>0.05).Conclusions The extract of Lindera aggregata can inhibit lung tissue inflammation and alleviate lung injury in LPS-in-duced ALI mice.The mechanism of action may be associated with the suppression of the NF-κB signaling pathway activa-tion.