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Objective To investigate the effect of matrine on gastric mucosal injury induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats and its mechanism. Methods A total of 75 Wister rats were randomly divided into a control group, a model group and three matrine-treated groups (100, 150 and 200 mg/kg). Except for the control group, the other groups were treated with MNNG to establish the models of gastric mucosal injury in the rats. After the models were successfully established, the rats in the three matrine-treated groups were administrated 100, 150, 200 mg/kg matrine, respectively, for successive 45 days. After the last administration, the body mass, daily intake of drinking water and dietary of rats were measured. And then the tissue samples were collected after the rats were sacrificed. The levels of interleukin 1β (IL-1β), IL-4, interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) were measured by ELISA in gastric mucosa. HE staining was used to observe the pathological changes of gastric mucosa tissue. Immunohistochemical staining was performed to evaluate the expression of vascular endothelial growth factor C (VEGF-C) and vascular endothelial growth factor receptor 3 (VEGFR3) in gastric mucosa. The protein levels of Bcl2, BAX, caspase-3, cytochrome C (Cyt-C), Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor κB p65 (NF-κB p65) were determined by Western blotting. Results The body mass, daily intake of drinking water and dietary increased in matrine-treated rats in comparison with the model group. In addition, compared with the model group, matrine significantly reduced the expression levels of VEGF-C, VEGFR3, BAX, caspase-3, Cyt-C, TLR4, MyD88 and NF-κB p65, and increase Bcl2 protein level in the gastric mucosa tissues. Conclusion Matrine can reduce gastric mucosal damage induced by MNNG in rats, which is related to the down-regulation of VEGF-C/VEGFR3 and NF-κB/TLR4 signaling pathway.

Background: National Comprehensive Cancer Network (NCCN) guidelines recommend video-assisted thoracoscopic surgery (VATS) anatomical lobectomy as the first choice for the treatment of resectable lung cancer. However, sublobar resection offers significantly better functional preservation compared with lobectomy for stage I lung cancer. At present, the inferiority of sublobar resection to lobectomy is still uncertain. Herein, we compared the prognoses of these two types of surgical treatment for stage I lung adenocarcinoma., Methods: Retrospective research was conducted on 258 patients with stage I lung adenocarcinomas who underwent VATS lobectomy and sublobar resection at the First Affiliated Hospital of Guangzhou Medical University between January 2009 and December 2011. VATS lobectomy was performed on 222 patients, and VATS sublobe resection was performed on 36 patients. Propensity score matching analyses were conducted on the two groups., Results: A total of 70 patients were matched in the two groups. No significant difference was observed between the lobectomy and sublobar resection groups after matching (P=0.137). The disease-free survival (DFS) of the two groups were 49.3 and 42.7 months, and their overall survival (OS) were 50.3 and 49.0 months (P=0.122). Further, stratified analysis showed no significant differences in DFS and OS between the two groups with stage Ia lung adenocarcinoma. Nevertheless, the DFS and OS of the two groups significantly differed in matched patients with stage Ib lung adenocarcinomas., Conclusions: Sublobar resection could achieve a similar prognosis to VATS lobectomy for stage Ia lung adenocarcinoma. Lobectomy should still be the first choice for the treatment of stage Ib lung adenocarcinoma.

Objective: To investigate the effect of intracellular-free Ca2+ concentration ([Ca2+]i) on injury following transient Mg(2+)-free treatment in vitro in developing cortical neurons., Methods: Embryo cortical neurons of rats cultured for 6 d and 17 d were directly exposed to Mg(2+)-free media, or pretreated with NMDA receptor antagonists or calcium channel antagonist before being exposed to Mg(2+)-free media. MTT assay was used to study the injury of neurons. [Ca2+]i were measured using fluo-3, a fluorescent calcium-sensitive dye and laser-scanning confocal microscope, and calculated by the fluorescent intensity., Results: Compared with control, MTT conversion rates decreased after transient (3 h) Mg(2+)-free treatment in neurons cultured for 6 d and 17 d in vitro, (59.1 +/- 6.87)% and (51.2 +/- 5.90)%, respectively. In neurons pre- and co-treated with 10 mumol.L-1 MK-801, 50 mumol.L-1 AP-5 and 10 mumol.L-1 nifedipine, MTT conversion rates were higher than those of neurons with only Mg(2+)-free treatment. Peak values of [Ca2+]i in neurons cultured for 6 d and 17 d were 2.4 +/- 0.23 and 3.2 +/- 0.32, respectively. Peak value of neurons 17 d in vitro was significantly higher than that of neurons 6 d in vitro (P < 0.05). In neurons pre- and co-treated with MK-801, AP-5 and nifedipine, [Ca2+]i were lower than those of neurons with only Mg(2+)-free treatment., Conclusion: Neuronal injury and [Ca2+]i changes following Mg(2+)-free-treatment-induced seizure were different between neurons 6 d and 17 d in vitro. It suggested that the age-dependent [Ca2+]i changes might play a role in an age-dependent manner of injury following Mg(2+)-free-treatment-induced seizure. NMDA receptor-Ca2+ pathway activation was crucial in the [Ca2+]i change and the cellular injury induced by Mg(2+)-free treatment.

Objective: To investigate whether the dopamine receptor D2 can express or can be induced to express in HNG1210-E, a monoclonal, telomerase-immortalized, human neural progenitor cell line., Methods: By means of RT-PCR, immuno-fluorescent staining, and fluo3 Ca2+ imaging to the expression of D2 mRNA and protein as well as the reaction to dopamine were demonstrated., Results: HNG1210-E cells could be induced to express D2 mRNA and its proteins. The induced cells also reacted to dopamine (5 mmol.L-1), which caused rapid rising of cytoplasm Ca2+., Conclusion: HNG1210-E cells can be induced to express D2 mRNA and functional proteins.

Objective: To study the neuroprotective effect and related mechanisms of triptolide., Methods: After being treated with 10(-10), 10(-9) mol.L-1 triptolide and/or 10, 50 mmol.L-1 glutamate for 24 hours, and the viability of PC12 was detected by MTT conversion, and the apoptosis rate was detected by AnnexinV-FITC and PI staining. In order to understand the underlying mechanism of the neuroprotective effect of triptolide, H2DCFDA and JC1 were used to detect the reactive oxygen species (ROS) and mitochondrial membrane potential., Results: Glutamate could induce PC12 necrosis and apoptosis. T10 at 10(-10) or 10(-9) mol.L-1 inhibited glutamate-induced cell death, ROS formation and decrease of mitochondrial membrane potential., Conclusion: T10 at 10(-10) or 10(-9) mol.L-1 can protect PC12 from the death induced by glutamate; and the underlying mechanisms may be involved in the inhibition of ROS formation and decrease of mitochondrial membrane potential.