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Aim To investigate the inhibitory effect of cistanche phenylethanol glycosides (CPhGs) on cardiac hypertrophy in rats caused by pressure overload and its related mechanism. Methods Male SD rats(n =70) were randomly divided into control group (Con), sham operation group (Sham), model group (Mod), positive control group (Vst), and different CPhGs dosage (125, 250, 500 mg • kg-1) groups. Cardiac ultrasound indexes, heart-weight to body-weight index (HWI), cardiac histopathological changes, and the area of myocardical cells (AMC) were detected. Plasma ET-1 and BNP levels were detected by Elisa, and protein expressions of phosphorylated PI3K(p-PI3K), PI3K, phosphorylated PKB (p-pKB) and PKB were detected by Western blot. Results Compared with Mod group, LVPWT, HWI, plasma ET-1, BNP and AMC decreased to different degrees. LVEDD, LVEF, LVFS, the protein expressions of myocardial tissues pPI3K and p-PKB increased to different degrees in CPhGs groups. Moreover, the indexes of CPhGs 250 and 500 mg • kg-1 groups were significantly improved compared to those of Mod group (P < 0. 05 or 0. 01). Compared with Vst group, there were no significant difference in CPhGs 500 mg • kg-1 group. Conclusions CPhGs could inhibit cardiac hypertrophy in rats induced by pressure overload, which might be related to the activation of PI3K/PKB signaling pathway.
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OBJECTIVE To study the effect of Cistanches phenylethanol glycosides (CPhGs) on acute lung injury in rats and the possible mechanism of action. METHODS Sixty SD rats were randomly divided into six groups: Normal control group, model group (lipopolysasccharide (LPS) 3 mg·kg-1], dexamethasone (Dex) positive control group (model+ Dex 2 mg·kg-1), model + CPhGs 125, 250 and 500 mg·kg-1 with 10 rats in each group. Each dose group of CPhGs was ig administered every day for 30 d, and the other three groups were ig administered with the same volume of distilled water for 30 d. The mode+Dex 2 mg·kg-1 group was ig given Dex 2 mg·kg-11 h before modeling. The rat model of acute lung injury was established after the rats in the other groups were intubated by the breath tube. Three hours after modeling, the rats were sacrificed by blood sampling from the abdominal aorta. The percentage of neutrophils in the whole blood, the activity of serum superoxide dismutase (SOD), glutathione (GSH) activity and the contents of malondialdehyde (MDA) and nitric oxide (NO) were detected. The contents of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and IL-6 in alveolar lavage fluid were detected. The wet/dry mass ratio (W/D) of the middle lobe of the right lung was calculated and the histopathological changes of the posterior lobe of the right lung were observed by HE staining. RESULTS Compared with normal control group, the percentage of neutrophils in the whole blood, W/D in the middle lobe of the right lung, the contents of MDA and NO in the serum were increased (P<0.05), but SOD, GSH, TNF-α and IL-6 were decreased in the model group (P<0.05). Compared with the model group, the percentage of neutrophils in the whole blood and W/D in right middle lobe of the right lung in the group of model+CPhGs 500 mg·kg-1 was decreased (P<0.05), but the contents of TNF-α and IL-6 in alveolar lavage fluid of rats decreased significantly, and histopathological observation showed that inflammation was alleviated to varying degrees. The activities of SOD and GSH in rat serum of the model + CPhGs 500 mg·kg-1 group were increased significantly (P<0.05), while the contents of MDA and NO were decreased significantly (P<0.05). CONCLUSION CPhGs have a protective effect against acute lung injury induced by LPS in rats, and its mechanism may be related to its antioxidant effect, alleviation of pulmonary edema and reduction of the release of inflammatory factors.
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OBJECTIVE： To identify chemical components of Forsythia suspense. METHODS： UPLC-Q-TOF-MS technology was used for the chemical components analysis of F. suspense. The determination was performed on ACQUITY UPLC BEH C18 column with mobile phase consisted of 0.1％ formic acid aqueous solution （A）- 0.1％ formic acid acetonitrile solution （B） with gradient elution， at the flow rate of 0.3 mL/min； the column temperature was set at 30 ℃； the sample size was 5 μL. Positive and negative ions were detected by electrospray ionization. The temperature of the ion source was 550 ℃； the atomizing gas was N2； the atomizing gas and the auxiliary pressure were 379.2 kPa； the air curtain pressure was 241.3 kPa； the decluster voltage was 80 V/－80 V； the collision energy was 35 eV/－35 eV； the mass scanning range was 80-1 500 Da. Peakview 2.0 software was used to screen the target components by the first-order mass spectrometry， and calculate the high-resolution and accurate molecular weight of each component， compare with the reference spectrum and related literature， or calculate the elemental composition of fragment ions in the second-order mass spectrometry， analyze their decomposition pathways， then infer the structure of compounds. RESULTS & CONCLUSIONS： 45 kinds of compounds were identified from F. suspense，which included 7 phenylethanol glycosides，5 lignans，5 terpenes， 12 flavonoids，7 organic acids，2 phenols，2 quinones，2 glycosides and 3 other components. There were 19 compounds identified for the first time in F. suspense. The study provides a reference for the in-depth study of the pharmacodynamic substance basis of F. suspense and the rapid qualitative and quantitative analysis of the components.
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Aim To investigate the effect of phenyle-thanol glycosides from Cistanche tubulosa(CPhGs) on the proliferation and activation of rrPDGF-BB induced HSC and their target points for resisting hepatic fibro-sis,to elucidate the molecular mechanism in molecular level, and provide basic data for the further develop-ment of new drugs. Methods HSCs were cultivated by CPhGs with different concentrations ( 0 , 3. 91 , 7. 81 , 15. 63 , 31. 25 , 62. 50 , 125. 00 , 250. 00 , and 500 mg ·L-1 ) and IC50 of CPhGs was determined. CPhGs with different concentrations ( 25 , 50 , 75 , 100 mg · L-1 ) were selected, and after the cells were stimulated with rrPDGF-BB, cell proliferation was determined by MTT. ERK1/2 ,α-SMA, c-fos, c-jun and Collagen I mRNA and Erk1/2 ,P-Erk1/2 and CollagenⅠprotein ex-pressions were assayed by RT-PCR and Western blot. Results CPhGs of ( 50 ~100 ) mg · L-1 concentra-tions groups could effectively inhibit rrPDGF-BB-medi-ated proliferation(P0. 05 ) . CPhGs of ( 25 ~100 ) mg · L-1 concentrations groups could inhibit ERK1/2 ,α-SMA,c-fos, c-jun and CollagenⅠmRNA levels, and also ob-viously inhibited Erk1/2 ,P-Erk1/2 and Collagen Ⅰ pro-tein expression on HSC. Conclusions CPhGs has the protective effect against hepatic fibrosis. The mecha-nism of this process may involve the interference with PDGF/ERK1/2 signaling pathway and inhibiting the activation and proliferation of HSC.