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Abstract Title:

[Baicalein attenuates acute lung injury induced by intestinal ischemia/reperfusion via inhibition of nuclear factor-κB pathway in mice].

Abstract Source:

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2017 Mar ;29(3):228-232. PMID: 28627342

Abstract Author(s):

Lei Chu, Fenyong Zhu, Wenjun Zhou, Zhongxiang Du, Jie Li, Xiaohong Wang, Lihui Wang, Anding Liu

Article Affiliation:

Lei Chu

Abstract:

OBJECTIVE: To investigate the effects of baicalein (Bai) on acute lung injury (ALI) induced by intestinal ischemia/reperfusion (I/R) and its mechanism in mice.

METHODS: Twenty-four male C57BL/6J mice were divided into three groups by random number table: namely sham group, I/R group and Bai+I/R group, with 8 mice in each group. Intestinal I/R induced lung injury model was reproduced by clamping superior mesenteric artery for 90 minutes, followed by reperfusion. Bai (100 mg/kg) was intraperitoneally injected 1 hour before ischemic challenge in the Bai+I/R group. The mice in sham group underwent the similar procedure with I/R group but without vascular occlusion. All mice were sacrificed at 4 hours of reperfusion, and blood was collected from inferior vena cava and lung tissues were harvested. Lung tissues were stained with hematoxylin-eosin (HE), and histological changes were examined under light microscope for pathological score. Lung wet/dry (W/D) ratio was calculated. Lung cell apoptosis was determined by TdT-mediated dUTP nick end labeling (TUNEL) technique. Serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of TNF-α and IL-6 in lung tissues were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). The protein expression levels of cytoplasmicinhibitory factor-α of nuclear factor-κB (IκB-α) and nucleus NF-κB were determined by Western Blot.

RESULTS: Under light microscope, a normal lung tissue structure was shown in the sham group and no evidence of obvious lung injury was found. In the I/R group, the alveolar structure was seriously damaged. The alveolar wall was widened and there was significant interstitial edema and leukocytes infiltration. In the Bai+I/R group, pathological damage was significantly decreased as indicated by reduced lung tissue edema and leukocytes infiltration. Compared with the sham group, the lung pathological scores, W/D ratio and cellular apoptosis in the I/R group were significantly increased. Both serum TNF-α and IL-6 contents and lung TNF-α and IL-6 mRNA expressions were significantly increased. Furthermore, I/R significantly resulted in a decrease of IκB-α in the cytoplasm and an increase of NF-κB in the nucleus. Notably, Bai treatment significantly attenuated ALI induced by intestinal I/R injury. Compared with the I/R group, the lung pathological scores and W/D ratio in the Bai+I/R group were significantly decreased (lung pathological score: 4.59±1.17 vs. 6.27±1.34, W/D ratio: 3.79±0.28 vs. 4.32±0.57), cellular apoptosis was significantly decreased [(4.85±2.47)% vs. (8.15±2.33)%], both serum TNF-α and IL-6 contents and lung TNF-α and IL-6 mRNA expressions were significantly decreased [serum TNF-α (pg/L): 124.18±30.49 vs. 167.72±38.65, IL-6 (ng/L): 1.65±0.69 vs. 2.43±0.57; lung TNF-α mRNA (2(-ΔΔCt)): 4.75±2.38 vs. 7.69±2.32, IL-6 mRNA (2(-ΔΔCt)): 16.45±4.39 vs. 27.69±6.82], additionally, Bai pretreatment significantly increased cytoplasmic IκB-α protein expression (gray value: 0.47±0.11 vs. 0.27±0.09), while decreased nuclear NF-κB protein expression (gray value: 0.57±0.13 vs. 1.07±0.14, all P<0.05).

CONCLUSIONS: Bai could attenuate intestinal I/R injury induced ALI via the inhibition of inflammation and apoptosis.

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