Role of tissue transglutaminase in the pathogenesis of diabetic cardiomyopathy and the intervention effect of rutin.

The aim of this study was to investigate the role of tissue transglutaminase (tTG) in the pathogenesis of diabetic cardiomyopathy (DCM) and the intervention effect of rutin. DCM was induced in rats by the injection of streptozotocin (STZ; 25 mg/kg). After a preliminary examination, the rats were randomly divided into four groups: Control (n=8), STZ-induced DCM (n=8), STZ + positive drug (captopril; n=6) and STZ + rutin (n=8) groups. The DCM model was evaluated using blood sugar values, serum enzyme levels, hematoxylin and eosin staining and Masson's staining, ex vivo. The protein and mRNA expression of tTG was assessed with immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The rat model of DCM was successfully established by STZ administration, and the expression levels of tTG were significantly increased in the DCM model. Following the injection of captopril or rutin, the blood sugar values, collagen content and expression levels of tTG were gradually reduced and serum enzyme levels were increased, as compared with those in the STZ-induced DCM group. In conclusion, tTG plays an important role in STZ-induced DCM. In addition, rutin may inhibit the expression of tTG and regulate myocardial injury in STZ-induced DCM.

Role of TGF-ß1 in human colorectal cancer and effects after cantharidinate intervention.

Effects of transforming growth factor-beta (TGF-ß) were investigated in human colorectal cancer, and the influence of cantharidinate in inhibiting TGF-ß1 expression was explored. Relationships among TGF-ß1 and sex, age, tumor size, tumor location, tumor stage were also analyzed. H and E and immunohistochemistry staining were employed to assess colorectal cancer and TGF-ß1 expression, respectively. Then, HCT-116 CRC cells were randomly divided into four groups, controls, no serum-treated, chemotherapy and cantharidinate-treated. Immunohistochemistry and real-time PCR were employed to assess the expression of TGF-ß1 in CRC cells. Our data showed that the expression of TGF-ß1 might be associated with tumor size and tumor location (P<0.05). The expression of TGF-ß1 in CRC groups was higher than in adjacent groups (P<0.05). In addition, the expression of TGF-ß1 in cantharidinate-treated group was much lower than in CRC group (P<0.05). Taken together, these results suggest that TGF-ß1 plays an important role in CRC development. Cantharidinate might inhibit the expression of TGF-ß1 and control the development of colorectal cancer.

Role of S100A3 in human colorectal cancer and the anticancer effect of cantharidinate.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality. The early diagnosis and treatment of CRC is the key to improving the survival of patients who may benefit from adjuvant chemotherapy. In the present study, the protein expression of S100A3 was observed in a cohort of 20 patients with cancer, which indicated that S100A3 activation was involved in tumorigenesis. In addition, the anticancer activity of cantharidinate was investigated using immunohistochemistry and quantitative polymerase chain reaction (qPCR) analysis. The protein expression of S100A3 was observed to increase by 2.4-fold in human CRC cells compared with the expression level in normal control cells (P<0.01). Cantharidinate inhibited the protein and gene expression of S100A3 in UCT-116 human CRC cells in vitro. These results suggested that S100A3 is important in human CRC. Cantharidinate has the potential to be considered as a novel adjuvant drug for controlling the expression of S100A3 in human CRC as it exhibits preventive effects.

Apoptosis of colorectal cancer UTC116 cells induced by Cantharidinate.

Effects of Cantharidinate on apoptosis of human colorectal cancer UTC-116 cells were investigated by means of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, H and E staining, flow cytometry, and Raman Spectra analysis. The results showed Cantharidinate to exert inhibitory action on proliferation of human colorectal cancer UTC-116 cells, inducing apoptosis, arresting cells in G1 phase, with decline of S and G2 phases. In addition, the results of Raman spectrum showed significant changes in the UTC-116 cells chemical structure with stretching after the application of Cantharidinate. Taken together, these results suggest that the treatment of human colorectal cancer with Cantharidinate may be associated with multiple molecular mechanisms for apoptosis. Furthermore, similar to fluorouracil, Cantharidinate should be considered as novel assistant drug for controlling the growth of human colorectal cancer UTC-116 cells.