10.3969/j.issn.2095-4344.2013.23.005

BACKGROUND: Intramyocardial transplantation of autologous umbilical cord-derived mesenchymal stem cells for repair of myocardial tissue damage is paid increasing attention in the cardiovascular field. OBJECTIVE: Human umbilical cord mesenchymal stem cells were isolated and cultured. Passage 2 human umbilical cord mesenchymal stem cells were treated with various concentratins of 5-azacytidine (2.5, 5, 10, 20, 40, 80 μmol/L) for 24 hours . After removal of 5-azacytidine, cells were cultured for another 4 weeks. RESULTS AND CONCLUSION: Before 5-azacytidine treatment, filament-like structures or particles were not observed in the cells, but the amount of cytoplasm was less and uniform, nuclear/cytoplasm ratio was high, cells exhibited typical fusiform appearance and grew in a swirl-like manner, and nucleolus was obvious. After treatment with 5-azacytidine for 24 hours, some cells died in each group, and typical fusiform appearance turned into stick-like or column-like appearance, especial y in the 40 and 80 μmol/L 5-azacytidine groups. Reverse transcription-PCR results showed that atrial natriuretic peptide and α-skeletal actin gene expression levels were detected on human umbilical cord mesenchymal stem cells after treatment with 2.5 or 40 μmol/L 5-azacytidine for 4 weeks or with 5, 10, 20 μmol/L 5-azacytidine for 1, 2, 3 and 4 weeks. These findings suggest that 5-azacytidine-induced human umbilical cord mesenchymal stem cells express the specific gene of myocardiocytes.

Sepsis is a common acute systemic infection,severe sepsis has a high rate of mortality,and its incidence rate is rising year by year.Due to the overproduction of free radicals in sepsis,microcirculation blood is drived disorder,multiple organ function can be impaired.This review describes the role of ascorbic acid in sepsis patients,which can reverse the oxidative stress injury rapidly through an eNOS-dependent mechanism,resisting platelet adhersion,preventing capillary embolism,resevering microcirculation blood flow,so as to improve patients' survival.

Sleep deprivation (SD) has a profound impact on the central nervous system, resulting in an array of mood disorders, including depression and anxiety. Despite this, the dynamic alterations in neuronal activity during sleep deprivation have not been extensively investigated. While some researchers propose that sleep deprivation diminishes neuronal activity, thereby leading to depression. Others argue that short-term sleep deprivation enhances neuronal activity and dendritic spine density, potentially yielding antidepressant effects. In this study, a two-photon microscope was utilized to examine the calcium transients of anterior cingulate cortex (ACC) neurons in awake SD mice in vivo at 24-hour intervals. It was observed that SD reduced the frequency and amplitude of Ca2+ transients while increasing the proportions of inactive neurons. Following the cessation of sleep deprivation, neuronal calcium transients demonstrated a gradual recovery. Moreover, whole-cell patch-clamp recordings revealed a significant decrease in the frequency of spontaneous excitatory post-synaptic current (sEPSC) after SD. The investigation also assessed several oxidative stress parameters, finding that sleep deprivation substantially elevated the level of malondialdehyde (MDA), while simultaneously decreasing the expression of Nuclear Factor erythroid 2-Related Factor 2 (Nrf2) and activities of Superoxide dismutase (SOD) in the ACC. Importantly, the administration of gallic acid (GA) notably mitigated the decline of calcium transients in ACC neurons. GA was also shown to alleviate oxidative stress in the brain and improve cognitive impairment caused by sleep deprivation. These findings indicate that the calcium transients of ACC neurons experience a continuous decline during sleep deprivation, a process that is reversible. GA may serve as a potential candidate agent for the prevention and treatment of cognitive impairment induced by sleep deprivation.

Objective To investigate the inhibitory effect and mechanism of lentinan on colitis-associated colorectal cancer (CAC) induced by azomethane (AOM)/dextran sulfate sodium salt (DSS) through the IL-6/ STAT3 pathway. Methods C57BL/6 mice were randomly divided into a control group, a model group, a low-dose group (0.865 mg/kg lentinan), a medium-dose group (1.73 mg/kg lentinan), and a high-dose group (3.46 mg/kg lentinan). Except the control group, CAC was induced by AOM/DSS in the other groups, and corresponding drugs were injected intraperitoneally during the modeling process. Body mass, disease activity index (DAI) score, colon length, and tumor number were compared among all groups. Hematoxylin–eosin staining was used to observe the pathological morphology of colon. ELISA was utilized to detect the IL-6, IL-1β, and IL-18 contents in serum. Western blot analysis was conducted to detect the expression levels of IL-6, p-STAT3, and c-Myc in colon tissues. Results The tumor number, DAI score, serum IL-6, IL-1β, and IL-18 contents and the expression levels of IL-6, p-STAT3, and c-Myc in the colon tissue of the model group were higher than those of the control group, while the body mass and colon length were lower than those of the control group (P<0.05). The pathological morphology of colon tissues showed adenocarcinoma formation. After different doses of lentinan intervention, the tumor number, DAI score, serum IL-6, IL-1β, and IL-18 contents and the expression levels of IL-6, p-STAT3, and c-Myc in colon tissues were all lower than those in the model group, while body mass and colon length were higher than those in the model group (P<0.05). The pathological morphology of colon tissues showed adenomas of different grades but no adenocarcinoma was found. Conclusion Lentinan inhibits CAC formation, and its anticancer effect is related to the inhibition of the IL-6/STAT3 pathway.