Curcumin inhibits heat-induced oxidative stress by activating the MAPK-Nrf2 / ARE signaling pathway in chicken fibroblasts cells.

Curcumin is a natural phenolic component of yellow curry spice, exhibits antioxidant and anti-inflammatory properties. In this study we investigated whether curcumin suppresses heat-induced apoptosis in chicken embryonic fibroblast cells (CEF) and the underlying mechanism. CEF cells line was divided into 6 groups (4 repetitions per group) including normal temperature group (NC), high temperature control group (H) and 4 experimental groups (H1(5 µmol/L), H2(10 µmol/L), H3(20 µmol/L) and H4(40 µmol/L)). Control groups were cultured in basic medium without Curcumin, while, the experimental groups were supplemented with 5, 10, 20 and 40 µmol/L, respectively. The experimental groups and H control group were cultured at 43 ℃ (95% air/5% CO2), whereas NC group cells were cultured at 37 °C. After 6, 12 and 24 h of culture, cells were collected for viability, proliferation, apoptosis, antioxidant status and gene expression analysis. Results showed that heat stress trigged the ROS production and induced the apoptosis, leading to decrease the cell viability and proliferation. The enzymatic activities of antioxidants (SOD, CAT, and GPX) were down-regulated. The expression of antioxidant enzyme (CAT, SOD1, SOD2, GSTO1, GSTT1 and GSTA3) and MAPK-Nrf2 pathway genes (Nrf2, Jnk, Erk and P38) were down-regulated under heats stress condition. While, the Curcumin treated groups had decreased ROS and MDA content. Down-regulation of the activity and expression of antioxidant enzyme induced by heat were also reversed by curcumin. Furthermore the up-regulation in expression of Nrf2, Jnk, Erk and P38 in supplemented groups revealed the involvement of MAPK-Nrf2 signaling pathway to alleviate oxidative stress induced by heat stress. This study demonstrates that curcumin has the ability to ease the oxidative damage through activating the MAPK-Nrf2 signaling pathway in CEF cells.

Navicularines A-C: New diterpenoid alkaloids from Aconitum naviculare and their cytotoxic activities.

Three new bisditerpenoid alkaloids, navicularines A-C (1-3), and three known ones (4-6), were isolated from the ground parts of Aconitum naviculare. Their structures were elucidated by spectroscopic methods. All the new compounds were tested against five cell lines (HL-60, SMMC-7721, A-549, MCF-7, SW480). It was found that navicularine B exhibited certain cytotoxic activities in vitro, with IC50 values of 13.50, 18.52, 17.22, 11.18, and 16.36µM, respectively.

Low-dose hyper-radiosensitivity in human hepatocellular HepG2 cells is associated with Cdc25C-mediated G2/M cell cycle checkpoint control.

PURPOSE: Although the significance of cell cycle checkpoints in overcoming low-dose hyper-radiosensitivity (HRS) has been proposed, the underlying mechanism of HRS in human hepatocellular cells remains unclear. Therefore, the aim of this study was to characterize HRS inhuman hepatocellular HepG2 cells and to explore the molecular mechanism(s) mediating this response. MATERIALS AND METHODS: HepG2 cells were exposed to various single doses of γ radiation (from 0 Gy to 4 Gy), and then were assayed at subsequent time-points. Survival curves were then generated using a linear-quadratic (LQ) equation and a modified induced repair model (MIRM). The percentage of cells in the G1, G2/M, and S phases of the cell cycle were also examined using propidium iodide (PI) staining and flow cytometry. Levels of total cell division cyclin 25C (Cdc25C) and phosphorylated Cdc25C were examined by Western blotting. RESULTS: Low-dose γ radiation (<0.3 Gy) induced HRS in HepG2 cells, while doses of 0.3, 0.5, and 2.0 Gy γ radiation significantly arrested HepG2 cells in the G2/M phase. While total Cdc25C levels remained unchanged after irradiation, levels of phosphorylated Cdc25C markedly increased 6, 16, and 24 h after treatment with 0.5 or 2.0 Gy radiation, and they peaked after 16 h. The latter observation is consistent with the G2/M arrest that was detected following irradiation. CONCLUSIONS: These findings indicate that low-dose HRS in HepG2 cells may be associated with Cdc25C-mediated G2/M cell cycle checkpoint control.

Anatomical basis and clinical research of pelvic autonomic nerve preservation with laparoscopic radical resection for rectal cancer.

The clinical effect of laparoscopic rectal cancer curative excision with pelvic autonomic nerve preservation (PANP) was investigated. This study evaluated the frequency of urinary and sexual dysfunction of 149 male patients with middle and low rectal cancer who underwent laparoscopic or open total mesorectal excision with pelvic autonomic nerve preservation (PANP) from March 2011 to March 2013. Eighty-four patients were subjected to laparoscopic surgery, and 65 to open surgery respectively. The patients were followed up for 12 months, interviewed, and administered a standardized questionnaire about postoperative functional outcomes and quality of life. In the laparoscopic group, 13 patients (18.37%) presented transitory postoperative urinary dysfunction, and were medically treated. So did 12 patients (21.82%) in open group. Sexual desire was maintained by 52.86%, un-ability to engage in intercourse by 47.15%, and un-ability to achieve orgasm and ejaculation by 34.29% of the patients in the laparoscopic group. Sexual desire was maintained by 56.36%, un-ability to engage in intercourse by 43.63%, and un-ability to achieve orgasm and ejaculation by 33.73% of the patients in the open group. No significant differences in urinary and sexual dysfunction between the laparoscopic and open rectal resection groups were observed (P>0.05). It was concluded that laparoscopic rectal cancer radical excision with PANP did not aggravate or improve sexual and urinary dysfunction.

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3.

MicroRNAs (miRNAs) function as essential post-transcriptional modulators of gene expression involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs have been deregulated in hepatocellular carcinoma (HCC). Here, we investigated the role of miR-141 in HCC. Decreased expression of miR-141 was observed in both HCC tissues and cell lines. Ectopic overexpression of miR-141 reduced proliferation, migration, and invasion of HCC cells. E2F transcription factor 3 (E2F3) was confirmed to be a target of miR-141 in HCC cells. Moreover, restoration of E2F3 significantly reversed the tumor suppressive effects of miR-141. Our results suggest a critical role of miR-141 in suppressing metastasis of HCC cells by targeting E2F3.

[Application of laparoscopic transanal coloanal anastomosis in sphincter-preserving surgery for low rectal cancer].

OBJECTIVE: To evaluate the efficacy of laparoscopic transanal coloanal anastomosis (modified Parks procedure) in sphincter-preserving surgery for low rectal carcinoma. METHODS: Clinical data of 65 low rectal cancer patients undergoing laparoscopic modified Parks procedure from March 2009 to April 2012 in our department were reviewed retrospectively. Fecal continence, urination and sexual function were evaluated. RESULTS: All the patients were followed up from 6 to 38 months after operation. Anastomotic leakage was found in 2 cases, anastomotic stricture in 3 cases, hepatic metastasis in 1 case. No local recurrence occurred. The ratio of satisfactory defecation function was 61.5% (40/65) in six months, 84.2% (48/57) in 1 year and 88.9% (40/45) in 2 years respectively. Urinary dysfunction was found in 7 patients (10.8%). Among 36 male patients, 7 (19.4%) presented erectile dysfunction and 10 (27.8%) ejaculation dysfunction. Among 29 female patients, sexual life of 19 (65.5%) was satisfactory. CONCLUSION: Laparoscopic modified Parks procedure in sphincter-preserving surgery for low rectal cancer can increase the ratio of sphincter-preserving, and improve the functional outcomes of defecation, sex and urination.

[Association between RET proto-oncogene polymorphisms and Hirschsprung disease in Chinese Han population of Hubei district].

OBJECTIVE: To establish the genetic background of exon2, exon13, exon11 and exon15 polymorphisms of RET proto-oncogene and study the possible involvement of RET proto-oncogene in the etiology of Hirschsprung disease (HD) in Chinese Han population surrounding Province HuBei. METHODS: The genotype and allele frequencies of RET proto-oncogene polymorphisms were identified by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLPS) in 94 HD patients and 122 control subjects. RESULTS: The genotype and allele frequencies of exon2 were AA 0.17, AG 0.72, GG 0.11, A 0.53, G 0.47 in control, and AA 0.61, AG 0.35, GG 0.04, A 0.78, G 0.22 in HD, and those of exon13 were GG 0.30, GT 0.52, TT 0.18, G 0.56, T 0.44 in control, and GG 0.49, GT 0.36, TT 0.15, G 0.67, T 0.33 in HD. There were significant differences in the two polymorphisms above between HD and control. The genotype and allele frequencies of exon11 were AA 0.05, AG 0.16, GG 0.79, A 0.13, G 0.87 in control and AA 0.02, AG 0.14, GG 0.84, A 0.09, G 0.91 in HD, the differences were not found between these two groups about this site. Exon15 were all of CC genotype in spite of control or HD. CONCLUSIONS: These data provide evidences for the contributions of exon2 and exon13 polymorphisms of RET proto-oncogene to susceptibility to HD in Chinese Han population surrounding province.