Breast cancer is the most common malignancy in women worldwide and pharmaceutical agents have therapeutic and preventive effects in breast cancer. The human epidermal growth factor receptor 2/neu is one of the most important oncogenes in human breast cancer. Prepubertal exposure to endogenous estradiol and a phytoestrogen, genistein (Gen), has been shown to reduce future breast cancer risk. Gen downregulates tyrosine kinase regulated protein expression and reduces prostate cancer. In this study, the effects of prepubertal exposure to Gen on rat mammary carcinogenesis and the erbB2/Akt signal pathway were investigated. Prepubertal female Sprague-Dawley rats were daily exposed to Gen at 125 mg/kg (Gen-1) and 500 mg/kg (Gen-5) from postnatal days 22-28. Subsequently, the rats were given a single dose of 100 mg/kg 7.12-dimethylbenz [a] anthracene on postnatal day 42 to induce mammary tumor. The mRNA expression of erbB2 and amplified in breast cancer 1 (AIB1) was detected by reverse transcription-polymerase chain reaction. The protein levels of proliferating cell nuclear antigen (PCNA), erbB2, phosphotyrosine protein, Akt, and p-Akt were detected by immunohistochemistry and Western blotting. The activity of protein tyrosine kinase (PTK) was detected by liquid scintillation counting. The percentage of rats with mammary tumors in breast cancer model (BCM), Gen-1, and Gen-5 was 71.43, 52.38, and 33.34%, respectively. The incidence of 7.12-dimethylbenz [a] anthracene-induced mammary tumors significantly decreased in Gen-5 compared with that in BCM. The mRNA levels of AIB1 and erbB2 and the protein levels of erbB2, p-Akt, and PCNA protein expression were downregulated for a long time in the mammary tumors in Gen-5 groups. The activity of PTK was also decreased for a long time. However, the total Akt protein expression did not change significantly among BCM, Gen-1, and Gen-5. Prepubertal exposure of Sprague-Dawley female rats to 500 mg/kg Gen can reduce later breast cancer risk and its protective effect is associated with persistent downregulation of the expression of erbB2, p-Akt, AIB1, and PCNA and with low PTK activity in the mammary tumor. Our results suggest that erbB2/Akt signaling plays a role in tumor formation and targeting erbB2/Akt signaling with prepubertal exposure to Gen may provide greater efficacy to the current therapies used to treat tumors.

Objective. To study the possible mechanism of ghrelin in heart failure and how it works. Method. In vitro results demonstrated that ghrelin alleviates cardiac function and reduces myocardial fibrosis in rats with heart failure. Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area. Results. In vitro experimental results prove that we have successfully constructed a rat model related to heart failure, and ghrelin can alleviate the heart function of heart failure rats and reduce myocardial fibrosis. In addition, ghrelin is closely related to the decrease of the expression levels of ERK, c-jun, and c-Fos, but it can also increase the expression of PTEN in the rat model; in vivo experiments proved that we successfully constructed an in vitro cardiac hypertrophy model, and the intervention of ghrelin would reduce the expression of hypertrophic memory and increase the surface area of cardiomyocytes, increase the expression level of PTEN, and reduce the expression levels of ERK, c-jun, and c-Fos, while the blockade of PTEN will increase the expression of hypertrophy genes and increase the cell surface area, while the blockade of ERK will increase the expression of hypertrophic genes, which in turn will make the cell surface area reducing. Conclusion. Ghrelin inhibits the phosphorylation and nuclear entry of ERK by activating PTEN, thereby controlling the transcription of hypertrophic genes, improving myocardial hypertrophy, and enhancing cardiac function.

Ceramic coatings were fabricated on pure magnesium in silicate electrolyte system by ultrasonic micro-arc oxidation (UMAO) process, and then silica sol (CSG) and HF-CSG treatment were carried out on micro-arc oxidation coatings. The corrosion potential (Ecorr) and corrosion current density (Icorr) of the compound coatings were analyzed by electrochemical corrosion workstation. The corrosive morphology of the coatings was observed by scanning electron microscopy (SEM). Results showed that the Ecorr of the coating with CSG and HF-CSG treatment increased by 55 mV and 69 mV respectively in comparison with that of single UMAO coating, and its Icorr reduced an order of magnitude, which had enhanced the corrosion resistance.