1.Significance of the detection of serum levels of matrix metalloproteinases -1,-2,-3 and -9 in thoracic aortic diseases and acute myocardial ischemia
Feng LIAN ; Song XUE ; Ritai HUANG ; Sha LIU ; Zhenlei HU ; Bo XIE ; Zhenyang DAI
Clinical Medicine of China 2011;27(12):1248-1250
Objective To evaluate the clinical significance of the change of serum matrix metalloproteinases (MMP)-1,-2,-3 and -9 in acute and chronic aortic diseases and acute myocardial ischemia.Methods The blood serum levels of MMP-1,-2,-3 and -9 were detected in 30 patients with acute aortic dissection,19 patients with chronic aortic dissection,19 patients with aortic aneurysm and in 12 patients with acute myocardial ischemia,as well as in 16 healthy individuals who served as the control group.Serum MMP levels were measured by using an ELISA technique.Results There were significantly higher levels of MMP-3 in patients with acute myocardial ischemia as compared to acute aortic dissection ( [19.10 ± 3.11 ] μg/L vs [11.89 ± 1.31 ] μg/L,P =0.02).Significantly lower levels of MMP-1 were found in healthy controls compared to the groups of patients ( [1.30 ± 0.56 ] μg/L vs [2.99 ± 0.78 ] μg/L in acute aortic dissection,P =0.03,[3.12 ±0.78] μg/L in chronic dissection,P =0.02,[3.01 ± 1.01 ] μg/L in thoracic aortic aneurysm,P =0.03 and [5.01 ± 0.98 ] μg/L in acute myocardial ischemia,P =0.01 ).Higher levels of M MP-1 and MMP-3 were detected on males.There was a positive correlation between MMP-1 and increasing age ( r =0.38,P < 0.05 ).In patients operated for acute type A aortic dissection,the levels of MMP-1,MMP-3 and MMP-9 increased immediately after surgery,while the levels of MMP-2 decreased.Twenty-four hours after surgery levels of MMP-1,-2 and -9 were almost equal to the preoperative ones( P > 0.05 ).Conclusion Measurement of serum MMP levels in thoracic aortic disease and acute myocardial ischemia is a simple and relatively rapid laboratory test that could be used as a biochemical indicator of aortic disease or acute myocardial ischemia,when evaluated in combination with imaging techniques.
2.Study on Mechanism of Linggan Wuwei Jiangxintang in Treating Acute Lung Injury
Quanwu DAI ; Yi LIU ; Gege ZENG ; Jiawei HE ; Zhenyang HUANG
Chinese Journal of Experimental Traditional Medical Formulae 2023;29(24):95-103
ObjectiveTo explore the action mechanism of Linggan Wuwei Jiangxintang on the treatment of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. MethodTraditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), GeneCards, DisGeNET, and Herb databases were combined with clinical data from Gene Expression Omnibus (GEO) to screen the key targets of Linggan Wuwei Jiangxintang in the treatment of ALI. The protein-protein interaction (PPI) network was constructed to screen the core targets, and gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were performed. The mouse ALI model was established by LPS induction to verify the effect and key targets of Linggan Wuwei Jiangxintang on the treatment of ALI. The expression levels of Toll-like receptor 4 (TLR4), nuclear transcription factor-κB p65 (NF-κB p65), and phosphorylated NF-κB p65 (NF-κB p-p65) in lung tissue were detected by Western blot. ResultThe analysis showed that the treatment of ALI with Linggan Wuwei Jiangxintang was related to 10 core targets such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and JUN, involving TNF signaling pathway, Toll-like receptor signaling pathway, NF-κB signaling pathway, etc. The animal experimental results show that Linggan Wuwei Jiangxintang can reduce lung injury, improve the pathological state of ALI mice, significantly reduce the expression of TNF-α and IL-6 in serum, increase the activity of total superoxide dismutase (T-SOD) and catalase (CAT) in lung tissue, and reduce the expression levels of JUN, TLR4, NF-κB p65, and NF-κB p-p65 proteins in lung tissue. ConclusionLinggan Wuwei Jiangxintang can inhibit LPS-induced inflammation and oxidative damage in ALI mice, and its mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway and the reduction of inflammatory factors such as TNF-α and IL-6.