Objective To investigate the myocardial expressions of protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling pathway and effective mechanism of Yiqi Huoxue Fang depending on model of myocardial ischemia.Methods The model of acute myocardial infarction (AMI) was established through ligation of left coronary anterior descending branch in SD rats, and randomly divided into model group, perindopril group, Qishen Yiqi Gutta Pills group, Yiqi Huoxue Fang group and sham-operation group, and all groups were given orally corresponding medications respectively 2 d after operation.The observation time points were set on the 7th d and 28th d.The changes of heart function and structure were detected by using ultrasonic testing, changes of myocardial pathomorphology were observed after HE staining, and expressions of Akt, mTOR, p-Akt and p-mTOR in infarction marginal zone were detected by using Western blot test, real-time fluorescence quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry technique in all groups.Results The level of left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) decreased significantly in model group compared with sham-operation group on the 7th d and 28th d (P<0.01).The level of left ventricular end-systolic volume (LVESV) increased significantly on the 7th d (P<0.01), and levels of LVESV and left ventricular end-diastolic volume (LVEDV) increased significantly (P<0.01) on the 28th d in model group.The levels of LVEF and LVFS increased and levels of LVEDV and LVESV decreased significantly in all medicated groups compared with model group (P<0.01).The thinner ventricular wall, less cardiomyocytes, disorder myocardial cells arrangement and inflammatory cell infiltration were observed in infarction marginal zone in model group, and disorder myocardial cells arrangement and less cardiomyocytes were observed in all medicated groups.The ratio of p-Akt/Akt and p-mTOR/mTOR increased (P<0.05), expressions of Akt m-RNA and mTOR m-RNA increased significantly (P<0.01), and levels of p-Akt and p-mTOR positive cell rates increased significantly (P<0.01) in model group.The ratio of p-Akt/Akt and p-mTOR/mTOR increased (P<0.05), expressions of Akt m-RNA and mTOR m-RNA increased (P<0.05 or P<0.01), and levels of p-Akt and p-mTOR positive cell rates increased significantly (P<0.05) in all medicated groups.Conclusion Yiqi Huoxue Fang can improve heart function and protect myocardial cells through activating cardiac self-protective mechanism-Akt/mTOR signaling pathway in rats with myocardial infarction.

Background Pneumoconiosis is the most serious occupational disease in China, and silicosis accounts for about half of it. Any intervention effect of physical exercise as the key and core of lung rehabilitation training on silicosis is still unclear. Objective To explore potential intervention effect of physical exercise on silicotic mice. Methods Forty SPF C57BL/6 male mice were randomly divided into four groups, 10 in each group, including a control group, a physical exercise group, a silicosis model group, and a silicosis model + physical exercise intervention group. Silicotic mouse model was established by using 50 μL SiO₂ suspension (200 mg·mL⁻¹). A treadmill was used to prepare mice receiving physical exercise at 0° inclination, 12.3 m·min⁻¹, 60 min·d⁻¹, 5 d·week⁻¹ for 4 weeks. Pathological morphology of lung tissues was evaluated after hematoxylin-eosin (HE) staining; deposition of collagen in lung tissues was evaluated after Van Gieson (VG) staining; expression of p-protein kinase R-like endoplasmic reticulum kinase (PERK) was detected by immunofluorescence staining; expressions of cyclin dependent kinase inhibitors (p21) and p-p38 mitogen activated protein kinase (p38) were detected by immunohistochemistry. The protein expressions of endoplasmic reticulum stress signal factors [p-inositol-requiring enzyme-1α (p-IRE-1α), p-PERK, and p-eukaryotic initiation factor-2α (p-eIF-2α)], senescence signal factors (p-p53, p21, and p16), mitogen-activated protein kinase (MAPK) signal factors [p-p38, p-extracellular regulated protein kinases (p-ERK), and p-stress-activated protein kinase (p-JNK)] were detected by Western blotting. Results After designed acute SiO₂ exposure, the images of micro computed tomography (CT) showed high density shadows in lung tissues of the silicotic mice and less shadows in lung tissues of the physical exercise intervention mice. After HE staining, the proportions of silicotic nodule area in lung tissues was (18.67±3.89) % in the silicosis model group, and significantly decreased to (8.78±1.05) % in the silicosis model + physical exercise intervention group (P<0.05). After VG staining, the proportion of collagen fiber area of lung tissues was (10.37±2.18) % in the silicosis model group, and significantly decreased to (4.35±0.89) % in the silicosis model + physical exercise intervention group (P<0.05). The results of immunofluorescence staining showed that in the silicosis model group, the expression of p-PERK increased at the location of silicotic nodules, while in the silicotic model + physical exercise intervention group, the expression of p-PERK decreased. The immunohistochemical staining results showed that the expression of p21 and p-p38 increased in the lung tissues of the silicosis model group; the expression of p21 and p-p38 decreased in the lung tissues of the silicosis model + physical exercise intervention group. The results of Western blotting showed that compared with the control group, the expression levels of p-IRE-1α (0.11±0.03), p-PERK (0.95±0.40), p-eIF-2α (3.53±0.91), p-p53 (1.78±0.07), p21 (1.98±0.10), p16 (1.26±0.17), p-p38 (0.41±0.09), p-ERK (0.42±0.05), and p-JNK (3.20±1.23) of the silicosis model group were all upregulated (P<0.05). Compared with the silicosis model group, the expression levels of p-IRE-1α (0.03±0.01), p-PERK (0.31±0.12), p-eIF-2α (0.30±0.06), p-p53 (0.76±0.08), p21 (0.18±0.11), p16 (0.70±0.24), p-p38 (0.03±0.00), p-ERK (0.19±0.03), and p-JNK (0.46±0.21) of the silicosis model + physical exercise intervention group were downregulated (P<0.05). Conclusion Physical exercise may alleviate pulmonary fibrosis in silicotic mice, and inhibit abnormal expressions of endoplasmic reticulum stress signal, MAPK signal, and senescent signal.