RESUMO
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.
RESUMO
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.