Objective Neurological diseases are closely associated with the apoptosis of neuronal cells .This article aims to study the inhibitory effect of taurine on the apoptosis of hippocampal neurons by activating Caspase 9 as well as its protective effect on the nervous system and its mechanisms . Methods Mouse hippocampal neuronal cells were randomly divided into four groups:control, injury and apoptosis, low-dose taurine protection, and high-dose taurine protection.The proliferation of the neuronalcells was observed, their apoptosis examined by MTT colorimetric assay, and the expression of Caspase 9 in different groups detected by immunofluorescence and Western blot. Results The injury and apoptosis group showed a poor proliferation of the hippocampal neuronal cells and decreased cell viability (A=0.102 ±0.025), significantly lower than the control group (relative A=0.643 ± 0.013), the low-dose taurine group (relative A=0.504 ±0.072), and the high-dose taurine group (relative A=0.452 ±0.029) ( all P<0 .05 ) .Immunofluorescence assay revealed significantly increased Caspase 9 activation in the injury and apoptosis group (A=61386.8 ±10083.6) compared with the control (A=4502.2 ±2518.1), the low-dose taurine (A=20077.4 ±4187.5), and the high-dose taurine group (A=13976.2 ±7044.1) (all P<0.05).Western blot showed a remarkably higher expression of Caspase 9 in in the injury and apoptosis group (A=1.23) than in the control (relative A=0.17), the low-dose taurine (A=0.21), and the high-dose taurine group (A=0.19) (all P<0.05). Conclusion Taurine can protect neuronal cells by inhibi-ting Caspase 9 activation.

Tumor drug resistance is currently one of the most difficult clinical problems. There are many theories on the mechanism of tumor drug resistance, and metabolic reprogramming is one of its mechanisms. Tumor cells undergo metabolic reprogramming to meet the energy requirements of proliferation, especially the changes in the glucose metabolism. This article reviews the glucose metabolism reprogramming-related enzymes and the associated small molecule inhibitors that reverse tumor drug resistance.

Objective: To determine the effects of ω-3 polyunsaturated fatty acids from different sources on glucolipid metabolism in type 2 diabetic patients with dyslipidemia. Methods: We recruited participants from the diabetes specialist clinic at the Guanlin hospital in Yixing city, Jiangsu Province from February 2017 to March 2017. A total of 180 subjects were randomly assigned to 3 g/day fish oil (FO), perilla oil (PO), or fish oil mixed with linseed oil (FLO) for 6 months. The basic conditions and fasting venous blood sample were obtained from each study subject at baseline, after 6 months of intervention. Serum glucose and lipid metabolism were investigated. Results: A total of 156 subjects aged (62.6±8.6) years completed the final follow-up after 6 months (FO,54 subjects; PO,52 subjects; FLO,50 subjects). Among them,59 patients (37.8%) were male. Serum glucose, glycated hemoglobin, C peptide, insulin and homeostasis model assessment-insulin resistance were not significantly different among the three groups after 6 months. Serum triglyceride decreased, whereas high-density lipoprotein cholesterol increased in FO [1.33 (1.05,1.93) mmol/L, (1.36±0.29) mmol/L, respectively] compared with PO [1.71 (1.23, 2.17) mmol/L, (1.23±0.22) mmol/L, respectively] and FLO [1.51 (1.12, 2.22) mmol/L, (1.29±0.30) mmol/L, respectively] (P<0.05). Serum low-density lipoprotein cholesterol and apolipoprotein B decreased in PO [(2.60±0.57) mmol/L,(0.96±0.23) g/L, respectively] compared with FO [(2.89±0.76) mmol/L, (1.07±0.30) g/L, respectively] (P<0.05). Serum lipoprotein(a) decreased in FLO [130.7 (63.3,270.6) mg/L] compared with FO [137.4 (58.7,333.2) mg/L] (P<0.05). Serum free fatty acid decreased in FLO [(0.43±0.15) mmol/L] compared with PO [(0.53±0.22) mmol/L] (P<0.05). Conclusion The effects of ω-3 PUFA from different sources on glucose metabolism in type 2 diabetic patients with dyslipidemia are similar. Each of them has a good application prospect in improving lipid metabolism.