Effects of traditional korean medicine Lurong Dabu Decoction on TLR4/WNT-5A signaling pathway in guinea pigs with cough variant asthma / 中国药理学通报

Aim To discuss the mechanism of Lurong Dabu Decoction on cough variant asthma. Methods Guinea pigs were divided into normal group(CON), model group(OVA), Lurong Dabu Decoction high-dose group(HIGH),low-dose group(LOW), and dexamethasone group(DEX)at random. The CVA model was established by smoking plus injection of OVA, aluminum hydroxide solution and nebulized inhalation to stimulate cough. Gguinea pigs were dissected 24 hours after the last challenge to obtain alveolar lavage fluid(BALF)and lung tissues. Immunoadsorption(ELISA)method was applied to detect the types of inflammatory cells and the content of inflammatory cytokines in BALF; HE and Masson staining of the middle lobe of the left lung were used to observe the pathological changes in lung tissues; immunohistochemical staining was used to observe TLR4 and WNT-5A protein expression and distribution of lung tissues; the protein extracted from the upper lobe of the left lung was used to measure the level of TLR4 and WNT-5A protein in lung tissues by Western blot; immunofluorescence was employed to measure the fluorescence intensity of TLR4 and WNT-5A in lung tissues; flow cytometry was used to detect IL-4 and IFN-γ in guinea pig lung tissues. Results Lurong Dabu Decoction could improve guinea pig airway inflammation, inhibit collagen fiber deposition, reduce the content of IL-4, IL-5, and IL-13 in BALF, and inhibit the protein expression of TLR4 and WNT-5A in lung tissues and increase IFN-γ levels in lung tissues while decreasing IL-4 levels. Conclusion Lurong Dabu Decoction may inhibit the occurrence of CVA through TLR4/WNT-5A signaling pathway.

Traditional Korean medicine Lurong Dabu decoction regulates airway remodeling through WNT5A and TLR4 signaling pathway / 中国药理学通报

Methods The model of heart failure after myocardial infarction was established by left coronary artery liga-tion in rats. Two weeks after modeling, all rats were randomly divided into model group, LGZGD group, and captopril group. Meanwhile sham operation group was set up. The rats were given continuous intragastric administration with drug or distilled water for 28 days, once a day. The behavioral signs of rats in each group were observed. The cardiac function of rats in each group was examined by echocardiography. Serum BNP and NT-ProBNP content were detected by enzyme-linked immunoassay; The changes of myocardial his-topathological and collagen fibers in rats were detected using sirius staining. The contents of oxidative stress index including ROS, SOD in myocardial tissue of rats in each group were observed by DCFH-DA fluorescent probe and Enzyme-linked immunoassay. The ultra-structure of mitochondria was observed by transmission electron microscopy. Expressions of apoptotic proteins ( mitochondrial CytC, cytoplasmic CytC) were detec- ted by Western blot. Expression of proteins related to the Nrf2/BNIP3 pathway were examined by immunoflu-orescence and Western blot. Results LGZGD could significantly improve the cardiac function of rats, reduce the contents of BNP and NT-ProBNP, inhibit the excessive deposition of collagen in myocardial interstiti-um, reduce ROS, increase the content of SOD, improve mitochondrial structure damage, up-regulate the expression of Nrf2 and nuclear translocation, and reduce the expression of BNIP3. Conclusions LGZGD can inhibit the ventricular remodeling and prevent the occurrence of heart failure after myocardial infarction. Its pharmacological effects are mainly related to regulating the Nrf2/BNIP3 pathway, activating Nrf2, promoting its nuclear transfer, and further down-regulating BNIP3 , protecting mitochondrial function, and reducing cardiomyocyte apoptosis.

Inhibition of salidroside on airway remodeling in asthmatic mice by modulating NF-κB/TGF-β1 signaling pathway / 中草药

Objective: To investigate the effects of salidroside on airway remodeling and NF-κB and TGF-β1 signal transduction pathway in asthmatic mice. Methods: Forty female BALB/c mice of clean grade were randomly divided into four groups (n = 10), such as control, egg protein (OVA) asthma, low-, and high-dose salidroside groups. OVA was used to establish the asthmatic mice model, and the left lung tissues of all mice were treated by HE, PAS, and Masson trichrome staining after the last excitation in 24 h. The right lung tissues were detected by enzyme linked immunosorbent assay (ELISA) to observe the expression levels of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid (BALF), by RT-PCR to investigate the expression level of TGF-β1 mRNA, and by Western blotting to detect the expression levels of TGF-β1 and NF-κB p65 proteins. Results: Compared with the control group, the inflammatory cell counts and the expression levels of IL-4, IL-5, and IL-13 in asthmatic model group were increased. The expression levels of TGF-β1 mRNA and NF-κB protein from lung tissues were significantly higher than those in the control group (P 0.05). Conclusion: Salidroside might inhibit the development of airway remodeling in asthmatic mice, and the mechanism might be partly achieved through the inhibition of NF-κB/TGF-β1 signal transduction pathway.