Zhangjiagang Aoyang Hospital Co., Ltd.

Breast cancer (BC) is one of the most common malignant tumors in women. Angelica sinensis polysaccharide (ASP) is one of the main components extracted from the traditional Chinese medicine Angelica sinensis. Research has shown that ASP affects the progression of various cancers by regulating miRNA expression. This study aimed to explore the specific molecular mechanism by which ASP regulates BC progression through miR-3187-3p. After the overexpression or knockdown of miR-3187-3p and PDCH10 in BC cells, the proliferation, migration, invasion, and phenotype of BC cells were evaluated after ASP treatment. Bioinformatics software was used to predict the target genes of miR-3187-3p, and luciferase gene reporter experiments reconfirmed the targeted binding relationship. Subcutaneous tumor formation experiments were conducted in nude mice after the injection of BC cells. Western blot and Ki-67 immunostaining were performed on the tumor tissues. The results indicate that ASP can significantly inhibit the proliferation, migration, and invasion of BC cells. ASP can inhibit the expression of miR-3187-3p in BC cells and upregulate the expression of PDCH10 by inhibiting miR-3187-3p. A regulatory relationship exists between miR-3187-3p and PDCH10. ASP can inhibit the expression of β-catenin and phosphorylated glycogen synthase kinase-3β (p-GSK-3β) proteins through miR-3187-3p/PDCH10 and prevent the occurrence of malignant biological behavior in BC. Overall, this study revealed the potential mechanism by which ASP inhibits the BC process. ASP mediates the Wnt/β-catenin signaling pathway by affecting the miR-3187-3p/PDCH10 molecular axis, thereby inhibiting the proliferation, migration, invasion, and other malignant biological behaviors of BC cells.

There is a special role for estrogens in preventing and curing cardiovascular disease in women. Soy isoflavone (SI), a soy‐derived phytoestrogen, has similar chemical structure to endogenous estrogen‐estradiol. We investigate to elucidate the protective mechanism of SI on myocardial ischemia/reperfusion (MI/R) injury. Female SD rats underwent bilateral ovariectomy. One week later, rats were randomly divided into several groups, sham ovariectomy (control group), ovariectomy with MI/R, or ovariectomy with sham MI/R. Other ovariectomy rats were given different doses of SI or 17β‐estradiol (E2). Four weeks later, they were exposed to 30 minutes of left coronary artery occlusion followed by 6 or 24 hours of reperfusion. SI administration significantly reduced myocardial infarct size and improved left ventricle function and restored endothelium‐dependent relaxation function of thoracic aortas after MI/R in ovariectomized rats. SI also decreased serum creatine kinase and lactate dehydrogenase activity, reduced plasma malonaldehyde, and attenuated oxidative stress in the myocardium. Meanwhile, SI increased phosphatidylinositol 3 kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS) signal pathway. SI failed to decrease infarct size of hearts with I/R in ovariectomized rats if PI3K was inhibited. Overall, these results indicated that SI protects myocardial ischemia/reperfusion injury in ovariectomized rats through increasing PI3K/Akt/eNOS signal pathway and decreasing oxidative stress.

Objective: To investigate the influence of laparoscopic ultrasound radio-frequency ablation (LURFA) on immune function of patients with liver cancer from T-cell subgroup cell count and serum immune factor transition.Methods: 37 cases of patients with primary liver cancer to be subjected to LURFA were selected as observation group, and 29 cases of healthy persons were selected as control group.The fasting venous blood was collected before and after treatment, and flow cytometer and ELISA kit were employed to detect T-cell subgroup cell count and serum immunity factor level.The immunity function change trend of patients and the related modulation mechanism of LURFA were analyzed.Results: Before treatment, the Ts cell count, Th2 cell secretion factor interleukin (IL)-4, IL-10 level, and tumor cell secretion factor sIL-2R and TGF-β levels in the observation group were significantly higher than those in the control group (P < 0.05), and T, Th, NK, CIK counts and Th1 cell secretion factor IL-2, interferon (IFN)-γ, and TNF-α levels were significantly lower than those in control group (P < 0.05).After treatment, the Ts cell count, Th2 cell secretion factor IL-4, IL-10 and sIL-2R, and TGF-β were significantly decreased (P < 0.05), and T, Th, NK, CIK counts, and Th1 cell secretion factor IL-2, IFN-γ, and TNF-α levels were significantly increased (P < 0.05).Conclusions: Based on the long-term stimulation of tumor cell secretion factors, the cell immunity level of peripheral blood of liver cancer patients is in inhibitory state, and auxiliary T cell transits from Th1 to Th2.LURFA can inhibit sIL-2R and TGF-β secretion through stimulating antigen presentation, so as to regulate Ts/Th and Th1/Th2 ratio, and enhance the cell immunity function of patients.