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The present study investigated the effect of rutin on high glucose-induced actin, α2, smooth muscle, aorta (ACTA2) and p38 protein expression in diabetic nephropathy (DN). Human mesangial cells were divided into a control group, high glucose-induced mesangial cell group, high glucose + captopril group, and high glucose + rutin group (low, middle and high doses of rutin). Cell viability, adenosine 5'-triphosphate (ATP) content, cell cycle, and ACTA2 and p38 protein expression were examined using MTT assay, ATP assay kit, flow cytometry and immunofluorescence staining in cultured human mesangial cells, respectively. Cell viability, ATP content, and ACTA2 and p38 expression increased significantly in high glucose-induced mesangial cells (P<0.05). However, at concentrations of 0.2, 0.4 and 0.8 µmol/l rutin was able to inhibit high glucose-induced human mesangial cell viability, ATP content, and ACTA2 and p38 expression and improve the cell cycle progression of mesangial cells. In conclusion, ACTA2 and p38 proteins may have important roles in DN. Rutin may inhibit the expression of ACTA2 and p38 and may be utilized in the prevention and treatment of DN.

The aim of the present study was to investigate the effect of rutin treatment on the expression of glycogen synthase kinase (GSK)-3β and tumor necrosis factor (TNF)-α in A549 human lung carcinoma cells. The A549 cells were divided into control, cisplatin and rutin (low, middle and high) groups. ELISA and western blot analysis of TNF-α expression, 4',6-diamino-2-phenylindole (DAPI) staining and GSK-3β immunofluorescence staining were used to investigate the effect of rutin in the human lung carcinoma cells, using cisplatin as a positive control. TNF-α expression was significantly higher in the rutin and cisplatin groups compared with the control group. Additionally, DAPI staining revealed that the number of apoptotic cells was higher in the rutin and cisplatin groups compared with the control group, and immunofluorescence showed that the expression of GSK-3β in the cisplatin and rutin groups was significantly higher compared with that in the control group. The results of the present study suggest that rutin promotes the TNF-α-induced apoptosis of A549 human lung carcinoma cells. Furthermore, rutin may be able to regulate the expression of GSK-3β protein in these cells.

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.

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.

The aim of this study was to explore the use of urantide as an antagonist of the urotensin II (UII) receptor, G protein-coupled receptor 14 (GPR14), to protect against atherosclerosis (AS) in rats. The AS rat model was induced by an intraperitoneal injection of vitamin D3 (VD3) into rats fed with a high-fat diet for four weeks. Urantide was then injected into the rats. Immunohistochemical staining, serum biochemical assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to investigate the expression of UII and its receptor GPR14 in the AS rat model. Four weeks after induction, pathological changes typical of AS were observed in the AS rat model. In the plaques of the aortic tunica intima and tunica media, expression of UII and GPR14 was observed. The protein and gene expression levels of UII and GPR14 in the model group were significantly increased compared with those in the normal group (P<0.01). Urantide ameliorated the pathological changes of AS in the rat model and reduced the gene and protein expression levels of UII and GPR14 (P<0.05 or P<0.01). UII is associated with AS and the UII receptor GPR14-specific antagonist, urantide, demonstrates the ability to protect against AS. Thus, this study provides new insight and experimental theories for the clinical application of urantide to treat AS.

The aim of this study was to investigate the role of the Rho/Rho associated coiled coil-forming protein kinase (Rock) signaling pathway in the pathogenesis of ischemic myocardial fibrosis (MF) in rats. The MF rat model was established using isoprenaline hydrochloride (ISO, 15 mg/kg). Rats were randomly divided into ten groups: a control group and ISO-treated groups at 2 h, 4 h, 6 h, 12 h, 24 h, 48 h, 72 h, 7 days and 21 days. The MF model was evaluated by serum enzyme levels, hematoxylin and eosin (H&E) staining and Masson's staining, ex vivo . The mRNA expression of RhoA and Rock I was assessed with reverse transcription-polymerase chain reaction (RT-PCR). The cell type was evaluated by immunofluorescent and immunohistochemical staining. The protein expression of Rock I was evaluated using western blotting and immunohistochemistry. MF was found to be more developed in the ISO-treated group compared with the control group. CD31 and vimentin expression in fibroblasts and endothelial cells were significantly increased. In addition, the mRNA and protein levels of RhoA and Rock I were significantly increased. In conclusion, activation of Rho/Rock accelerates the degree of ischemic MF. Inhibition of Rho/Rock may be a novel therapeutic strategy for the prevention of ischemic MF.