Astragaloside II alleviates the symptoms of experimental ulcerative colitis in vitro and in vivo.

BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory intestinal disease, and its morbidity is rising worldwide. Previous study indicated that astragaloside II (AS II), a monomeric compound, was used to treat bowel disease. However, the effects of AS II on UC remains unclear. Thus, this study aimed to investigate the therapeutic effects of AS II on experimental UC in vitro and in vivo. METHODS: CCD-18Co cells were stimulated by 1 µg/mL LPS to mimic UC in vitro. In addition, dextran sulfate sodium (DSS)-induced UC mouse model was established in vivo. CCK-8 assay was used to detect cell proliferation in vitro. Moreover, the concentrations of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin 1ß (IL-1ß), nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in CCD-18Co cells and colon tissues were determined by ELISA, respectively. Meanwhile, the expressions of hypoxia-inducible factor 1α (HIF-α), phospho-inhibitor of NF-κB (p-IκB) and phospho-NF-κB p65 (p-p65) were detected by western blotting in vitro and in vivo, respectively. RESULTS: In this study, the levels of pro-inflammatory cytokines TNF-α, IL-1ß and IL-6 were significantly increased in lipopolysaccharide (LPS)-stimulated CCD-18Co cells. However, LPS-induced inflammatory response was markedly alleviated by AS II. In addition, LPS-induced HIF-α, p-IκB and p-p65 proteins increases were markedly ameliorated by AS II treatment. Moreover, AS II reduced disease activity index (DAI) scores and increased the colon lengths in DSS-treated mice. Meanwhile, AS II decreased the levels of IL-6, TNF-α, IL-1ß, NO, MPO and MDA, and increased the level of SOD in colon of DSS-treated mice. Furthermore, AS II downregulated the expressions of HIF-α, p-IκB and p-p65 in DSS-induced UC in mice. CONCLUSION: Our findings indicated that AS II could alleviate inflammatory response in LPS-induced CCD-18Co cells and in DSS-induced UC in mice. In conclusion, AS II may serve as a potential agent for the treatment of UC.

MicroRNA-362 Inhibits Cell Proliferation and Invasion by Directly Targeting SIX1 in Colorectal Cancer.

PURPOSE: Colorectal cancer (CRC) is the third most common cancer in China and poses high morbidity and mortality. In recent years, increasing evidence has indicated that microRNAs played important functions in the occurrence and development of tumors. The purpose of this study was to identify the biological mechanisms of miR-362 in CRC. MATERIALS AND METHODS: Quantitative real-time PCR was carried out to assess the expression of miR-362 and SIX1. The Kaplan-Meier method was employed to evaluate the 5-year overall survival of CRC patients. The proliferative and invasive abilities of CRC cells were assessed by MTT and transwell assays. RESULTS: miR-362 was significantly decreased in CRC tissues and cell lines, compared to the normal tissues and normal cells. A significant connection was confirmed between the overall survival of 53 CRC patients and low expression of miR-362. Downregulation of miR-362 inhibited the proliferation and invasion through binding to the 3'-UTR of SIX1 mRNA in CRC. Additionally, we discovered that SIX1 was a direct target gene of miR-362 and that the expression of miR-362 had a negative connection with SIX1 expression in CRC. SIX1 could reverse partial functions in the proliferation and invasion in CRC cells. CONCLUSION: miR-362 may be a prognostic marker in CRC and suppress CRC cell proliferation and invasion in part through targeting the 3'-UTR of SIX1 mRNA. The newly identified miR-362/SIX1 axis provides insight into the progression of CRC.

Effect of hyperbaric oxygen on the process of hypertrophic scar formation in rabbit ears.

OBJECTIVE: To explore the influence of hyperbaric oxygen on scar formation in rabbit ears. METHODS: A total of 20 New Zealand rabbits were selected to establish the hypertrophic scar model on the ears. The rabbits were randomly divided into control group and experimental group (7d, 14d, 21d, and 28d group according to different HBO treatment days),each experimental group received hyperbaric oxygen treatment after the operation at the same time everyday for 1 hour. After the day 29, the scars were collected. Histomorphological change in scars was observed by hematoxylin-eosin staining, Masson staining, and transmission electrical microscope. The expression of bax, bcl-2, and the cell apoptosis rate was detected by immunohistochemical method. RESULTS: (i) Both number of fibroblast and amount of collagen fibrils in experimental group were significantly reduced compared with those in control group. In Masson staining, arrangement of collagen fibrils in experimental group was much more irregular and coarse than control groups. (ii) HI value can be found much smaller in the experimental groups than the control (P < .05). Among the four experimental groups, there is significant difference among 7d, 14d, and 21d groups (P < .05), while there is no difference between 21d and 28d groups (P > .05). (iii) Expression of Bax could be detected up-regulated in experimental group (P < .05). While the expression of Bcl-2 is detected significantly down-regulated in experimental group than that in control group (P < .05). Compared with the 7d group, the expression of Bax and Bcl-2 has significant difference in 14d group (P < .05), and the expression of this two factors in 21d group has significant difference comparing with 14d group(P < .05),but there is no significant difference between 28d group and 21d group(P > .05). (iv) Significant difference of cell apoptosis rate can be detected between the experimental groups and the control group (P < .05). Among the four experimental groups, there is significant difference among 7d, 14d, and 21d groups (P < .05), while there is no difference between 21d and 28d groups (P > .05). CONCLUSION: The hyperbaric oxygen can up-regulate bax/bcl-2 value, increase the cell apoptosis rate, and inhibit the early hypertrophic scar in rabbit ears.