ROS-mediated oxidative stress involved in a variety of cellular signal transduction, FOXO3a transcription factor is an intersection in regulating a variety of cellular oxidative stress. FoxO3a has been extensively studied in regulating oxidative stress because of its rather complex and pivotal regulation of cell proliferation, cell cycle arrest, ROS scavenging and apoptosis. This review will elucidate the FOXO3a’s regulatory mechanisms and describe the target genes involved. It will also provide the clinical significance and strategies to target FOXO3a to regulate oxidative stress.

Aim To observe the effects of low concentration ouabain(OUA)on intracellular calcium concentration ([Ca2+]i) were investigated in guinea pig ventricular myocytes.Methods The guinea-pig ventricular myocytes were obtained by enzymatic dissociation technique, then were incubated with Fluo3-AM. The Fluo3-AM fluorescent signal was detected with confocal laser scanning microscopy. The change of [Ca2+]i was represented by the percentage of fluorescence intensity change [(FI-FI0)/FI0,%] (FI: fluorescent intensity after addimg OUA, FI0: control). Results In normal Tyrode,s solution and Ca2+-free Tyrode′s solution.OUA (1?10-9~1?10-6 mol?L-1)elevated [Ca2+]i in a concentration-dependent manner, in normal Tyrode′s solution by 16.7?6.8(P0.05).Genistein (GST) (1、10、50、100 ?mol?L-1)abolished the OUA-induced increases in[Ca2+]i in a concentration-dependent manner by 17.5?3.1、14.2?8.9、0.8?7.6(P

Abstract Alzheimer's disease (AD) is a neurodegenerative disease characterized by deposition of β-amyloid (Aβ). Liver X receptors (LXRs), a member of the nuclear receptor transcription factor superfamily, are widely expressed in brain, which may be involved in the development and progression of AD. Based on the international and national publications pertaining to the association between LXRs and AD from 2010 to 2022, this review summarizes the advances on the involvement of LXRs in the regulation of cholesterol metabolism, inflammatory response and synapse formation in the pathogenesis of AD was reviewed, so as to provide insights into the prevention and treatment of AD.

Aim To introduce an improved method of Langendorff perfusion of the isolated rat heart that is easy to determine the termination of digestion.Methods Hearts were excised quickly from anesthetized SD rats.After the perfusate was free of blood,the solution was changed to perfusion buffer(0.6% Collagenase B,0.6% BSA,30 ?mol?L-1 Ca2+ in Tyrode solution)at 37℃.Hearts were isolated by traditional and improved Langendorff perfusion.Individual myocardial cell was measured by video-based motion edge-detection system(IonOptix,USA).Results One group of heart was digested by traditional Langendorff perfusion for 13~16 min.The termination of digestion could not be judged properly by this method.The nature and quality of the cardiocytes were various.The cardiocytes could not keep their survival and viability when exposed to Tyrode Solution with 1.8 mmol?L-1 Ca2+.Another group was digested by improved Langendorff perfusion.More than 80% survival cardiac ventricle myocytes could be obtained by improved Langendorff perfusion.Moreover,about 50% cardiac myocytes exposed to Tyrode solution with 1.8 mmol?L-1 Ca2+ could retain rod-shaped and be used to contraction research.The contraction of cardiocyte was stabile within 1 000 s.Conclusion Cardiac myocytes disassociated from improved Langendorff perfusion can be used in these studies of detecting contraction and relaxation.This method is economical and easy to control.The beginners are able to acquire the technological method over a short-term practice.

OBJECTIVE To observe the protection of vitamin C on the cardiac injury induced by 50 nm titanium dioxide inmice.METHODS Kunming mice were ad mistered by ig of vitamin C 100,200 and 400 mg·kg -1 for 2 d.And then the mice were ad mistered by ig of nano-TiO2 2 g·kg -1 and vitamin C (100.0,200.0 and 400.0 mg·kg -1 )for 3 d,the interval of treatment with nano-TiO2 and vitamin C was 4 h.The mice were scarified 24 h later after the last ad ministration.Electrocardiogra m (ECG)was determinated by physiological recorder.The myocardial enzy mes activities in serum and superoxide dismutase (SOD)and glutathione peroxidase(GSH-Px)activities in serum and myocardial tissue were determinated by bioche mical method.Cometassay was used to detect the DNA da mage of the heart. Heart tissue was used for histopathological exa mination by HE staining.RESULTS Co mpared with the control,ECG showed higher S-T and T-wave a mplitude of nano-TiO2 2 g·kg -1 (P<0.05).The myocar-dial enzy mes activities significantly increased and activities of SOD and GSH-Px significantly decreased in nano-TiO2 group,compared with the control group(P <0.05).Cometassay showed that olive tail mo ment (OTM)was significantly increased after nano-TiO2 2 g·kg -1 ,compared with the control group (P<0.05).The histopathology showed ede ma of myocardial cells,myofibril disorders and increasing infla mmatory cells.Vita min C 100,200 and 400 mg·kg -1 can decrease S-T in ECG,OTM,myocardial enzy mes activities,increase the SOD and GSH-Px activities in serum and myocardial tissue;reduce myocardial hypertrophy and infla mmatory cells.CONCLUSION nano-TiO2 can induce myocardial injury inmice and vitamin C can alleviate the da mage.The mechanism may be associated with the antioxidant ability of vitamin C inmyocardial tissue.

Objective: This study was to investigate the effects of MEHP on isolated rat heart and explore its mechanism. Methods: The experiments were performed with Langendorff-perfused rat heart with a Langendorff apparatus. 35 SD rats were used in the experiment and there were 5 rats per group. MEHP at doses of 3.125, 6.250, 12.500 and 25.000 μmol/L were given to the hearts for 25 minutes. Effects of NAC at concentration of 5 mmol/L were evaluated by co-treatment with 12.500 or 25.000 μmol/L MEHP. Data was collected per 5 minutes for 25 minutes. The heart rate, LVDP, LVEDP, dp/dtmax, and dp/dtmin were measured and analyzed using a PL3508 Data Acquisition and Analysis System. 200 waves at least were required each time. LDH contents in heart lavage fluid were determined by photometric assays using the automated biochemical analyzer. A section of the heart tissue was used for histopathological examination. DCFH-DA method was used to detect the levels of reactive oxygen species in different groups of heart tissues. Results: There was a concentration dependent decrease of heart rate (P<0.05) . At concentrations of 6.250, 12.500 and 25.000 μmol/L, MEHP significantly decreased the LVDP, dp/dtmax and dp/dtmin (P<0.05) , and this decrease is more pronounced with perfusion time. As the MEHP was given up to 6.250, 12.500 and 25.000 μmol/L, a statistical significance was found in the increase of LVEDP (P<0.05) . For dp/dtmin, a significant increase was observed at the concentration of 3.125 μmol/L when perfused with 10 and 15 min (P<0.05) , but this increase disappeared over time. LDH in cardiac perfusate increased as the MEHP given a higher concentration (P<0.05) . Compared with the control group, Histopathological analysis showed edema of myocardial tissue and cells, and inflammatory cells infiltration and myocardial cells necrosis were obvious in the MEHP perfusion groups. Myocardial ROS levels of the four MEHP treatment groups were all significantly higher than that of control group (P<0.05) . These heart damage induced by MEHP could be attenuated by NAC in different degrees. Conclusion MEHP can induce damage to myocardial tissue of isolated rat heart and one possible mechanism is the oxidative stress