Effects of tanshinone II A on the myocardial hypertrophy signal transduction system protein kinase B in rats.

OBJECTIVE: To study the effect of tanshinone II A on the cell signal transduction system protein kinase B (Akt) in rats with hypertrophy of the myocardium induced by partial constriction of the thoracic aorta. METHODS: Rat models of myocardial hypertrophy were established by the thoracic aorta partial constriction method. Forty-eight rats were randomly divided into the sham-operative group, the model group, the valsartan treatment group, and the low-, medium-, and high-dose tanshinone treatment groups. The heart mass index (HMI), left ventricular mass index (LVMI), ejection fraction (EF), left ventricular posterior wall (LVPW), and interventricular septal thickness (IVS) were detected by high-frequency ultrasonography. The myocardial fiber diameter (MFD) was detected by HE staining, and the contents of p-Akt and p-Gsk3beta in the myocardium were detected by Western blot. RESULTS: Compared with the sham-operative group, the levels of HMI, LVMI, LVPW, IVS, and MFD were increased respectively in the other groups (P<0.05); the contents of p-Akt and p-Gsk3beta were also increased in the other groups. Compared with the model group, the levels of HMI, LVMI, LVPW, IVS, and MFD were decreased respectively in all treatment groups (P<0.05); the contents of p-Akt and p-Gsk3beta were decreased in all treatment groups as well. There was no significant difference, however, among the low-, medium-, and high-dose tanshinone treatment groups and the valsartan treatment group (P>0.05). CONCLUSION: Tanshinone II A can prevent myocardial hypertrophy by its action on the protein kinase B (Akt) signaling pathway.

[Effects of rotundine injection on nitric oxide synthase in tissues of different organs after ischemia/reperfusion of brain in rats].

OBJECTIVE: To explore the protective effect of rotundine injection on lung, liver and kidney damages after cerebral ischemia/reperfusion (I/R) injury in rats based on the activity changes of nitric oxide synthase (NOS). METHODS: Seventy-six rats were randomly divided into three groups: sham operation group, I/R injury group and treatment group, and determinations were done at five different time points. The cerebral I/R models were reproduced by improved 4 vessels occlusion method. The activities of NOS in the lung, liver and kidney were measured in all the rats at 2, 6, 12, 24 and 48 hours after reperfusion. RESULTS: Compared with sham operation group, the activities of total NOS (tNOS) were significantly increased at 2, 12 and 24 hours in I/R injury group (P<0.05 or P<0.01), with the peak value at 12 hours (all P<0.01). The activities of constitutive NOS (cNOS) were increased significantly at 2 hours (all P<0.05), and those of induced NOS (iNOS) were increased at 12 hours (all P<0.01). The activities of iNOS were still high at 24 hours (all P<0.05), and approached the levels of sham operation group at 48 hours. Compared with I/R injury group, the activities of cNOS in various organs increased much higher at 2 hours in treatment group (all P<0.05). But those of iNOS were significantly decreased after 12 hours (P<0.05 or P<0.01). CONCLUSION: The various types of NOS play different roles in the lung damages after brain I/R injury at different stages in rats. Rotundine injection can ameliorate the damages by modulating the activities of different types of NOS.