Objective To investigate the effect and possible mechanism of Emodin on Doxorubicin(DOX)-induced cardiotoxicity.Methods H9C2 cells were preincubated with low,medium and high doses(5,15 and 25 μmol·L-1)of Emodin for 8 h,and then cardiomyocytes were treated with 2.5 μmol·L-1 DOX for 16 h to establish a cardiotoxic injury model.MTT assay was used to detect the cell survival rate.The levels of cardiac troponin(cTnT),lactate dehydrogenase(LDH),creatine kinase(CK),superoxide dismutase(SOD),reactive oxygen species(ROS),malondialdehyde(MDA),reduced glutathione(GSH),glutathione peroxidase(GSH-Px)and the activities of Caspase-3 and Caspase-9 in H9C2 cells were detected by kit;RT-qPCR was used to detect miR-29a-5p and vascular endothelial growth factor-B(VEGFB)expression levels.The expression levels of VEGFB protein and other apoptosis-related factors were detected by Western blot.After transfection of miR-29a-5p mimics and inhibitors,the targeting of VEGFB to miR-29a-5p was detected by RT-qPCR and Western blot.H9C2 cells were transfected with miR-29a-5p mimics,Under the dose of Emodin 15 μmol·L-1,the activity of H9C2 cells was detected by MTT method,and the expression levels of miR-29a-5p and VEGFB were detected by RT-qPCR and Western blot.Results Compared with the DOX group,Emodin low,medium and high dose groups significantly increased the activity of H9C2 cells(P<0.05,P<0.01),and decreased the levels of cTnT,LDH and CK(P<0.05,P<0.01);RT-qPCR indicated that the expression level of miR-29a-5p decreased significantly and the expression level of VEGFB increased significantly(P<0.05,P<0.01);The levels of ROS and MDA decreased significantly,and the levels of GSH and GSH-Px increased significantly(P<0.05,P<0.01);TUNEL positive cells decreased significantly,and the activities of Caspase-3 and Caspase-9 decreased significantly.Western blot showed that the expression level of VEGFB increased significantly,the expression level of apoptosis-related factor Bax decreased significantly,and the expression levels of Bcl-2 and Bcl-xl increased significantly(P<0.05,P<0.01).After transfection with miR-29a-5p mimics and inhibitors,the expression of VEGFB decreased and increased respectively(P<0.05,P<0.01).After transfection of miR-29a-5p mimics and treatment with Emodin 15 μmol·L-1 of H9C2 cells,the significant decrease in the activity of H9C2 cells induced by DOX was reversed,and the significant decrease in the expression level of VEGFB was also reversed(P<0.05,P<0.01).Conclusion Emodin significantly reduces DOX-induced cardiotoxicity by regulating miR-29a-5p/VEGFB-mediated cardiomyocyte apoptosis.

Objective To investigate the microstructural changes of temporal lobe epilepsy(TLE)in patients with sleep disorders based on diffusion kurtosis imaging(DKI).Methods This research prospectively included 38 TLE patients(case group)and 20 healthy controls(HC)(HC group).Participants used sleep questionnaires to evaluate their sleep status.All TLE patients were divided into groups with and without sleep disorders according to the diagnostic criteria and scale scores of sleep disorders.The mean kurtosis(MK),mean diffusivity(MD),and fractional anisotropy(FA)of the relevant region of interest(ROI)were measured by DKI sequence.The differences of sleep quality scores and DKI parameters between groups were further compared via independent samples t-test and one-way analysis of variance.Results The Epworth sleepiness scale(ESS),Athens insomnia scale(AIS),and Pittsburgh sleep qual-ity index(PSQI)scores of TLE patients with sleep disorders were significantly higher than those of HC group(P＜0.05).The FA and MK values in TLE patients were significantly lower than those in HC group,while the MD value of TLE patients were substan-tially higher than that of HC group(P＜0.05).The values of MK and FA in left TLE patients with sleep disorders were significantly lower than those of without sleep disorders(P＜0.05),while there was no significant difference in MD value between the two groups(P＞0.05).MK value of right TLE patients with sleep disor-ders was significantly lower than that of without sleep disorders(P＜0.05),however,there were no significant differences in MD and FA values between the two groups(P＞0.05).Conclusion Quantitative DKI analysis revealed differences in DKI parameters in TLE patients combined with sleep disorders,inferring a specific white matter fiber damage in this group and providing imaging data to support the personalized treatment and prognostic assessment of these patients.

ObjectiveTo establish a nude mouse model of type 2 diabetes mellitus （T2DM） and pancreatic cancer that allows dynamic observation of tumor formation process and facilitates in vivo research. MethodsAt first， human pancreatic cancer PANC-1 cells were transfected with lentiviral vector GV260 to construct the pancreatic cancer cell line PANC-1-Luc with stable expression of firefly luciferase. Then， 36 specific pathogen-free nude mice were randomly divided into control group with 12 mice and model group with 24 mice （nude mice with T2DM and pancreatic cancer）. The mice in the control group were fed with breeding diet and were then given ectopic subcutaneous implantation of PANC-1-Luc cells， and those in the model group were first given high-fat diet and intraperitoneal injection of 1% STZ， followed by ectopic subcutaneous implantation of PANC-1-Luc cells. The fluorescence in vivo imaging system and the manual measurement method were used for simultaneous and dynamic monitoring of the growth of pancreatic cancer in nude mice in the two groups， and the tumor growth curve was plotted to investigate the correlation between fluorescence value and tumor volume. Subcutaneous tumors and pancreatic islets were observed under a microscope to verify whether the model was successfully established， and immunohistochemistry was used to measure the expression of Ki-67 in tumor tissue to investigate the influence of hyperglycemia on the growth of pancreatic cancer in nude mice. The independent-samples t test was used for comparison of normally distributed continuous data between groups， and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between groups. ResultsThe optimal virus titer was determined as 5×10⁷ TU/mL for the stable transfection of lentiviral vector in PANC-1 cells， and the optimal concentration selected with puromycin was 20 μg/mL， with an optimal selection time of 9 days. The fluorescence value of PANC-1-Luc cells was linearly and positively correlated with the number of cells， with the linear equation of y=42.56x－42 504 （r=0.977， P=0.004）. The blood glucose value of T2DM nude mice was 23.05 （19.25‍ — ‍26.40） mmol/L， with a blood glucose level of >11.1 mmol/L in each nude mouse， and there was a significant difference in blood glucose value between the T2DM nude mice and the control nude ［6.15 （5.20‍ — ‍7.30） mmol/L］ （Z=-8.45， P<0.001）. Compared with the control group， the model group had reductions in the number and volume of pancreatic islets， with irregular shapes and unclear boundaries， and pathological examination confirmed that the xenograft tumor was pancreatic cancer tissue， which showed that the model was established successfully. In the model group， there was a linear positive correlation between subcutaneous tumor size and fluorescence values， with the linear equation of y=232 348 691x－8 258 608 （r=0.911， P=0.031）. The model group had a significantly higher positive rate of Ki-67 than the control group （50.333%± 7.808% vs 15.917%±4.055%， t=13.55， P<0.001）， suggesting rapid tumor proliferation in the model group. ConclusionThe T2DM nude mouse model of pancreatic cancer established in this study can simulate the pathological process of the development and progression of pancreatic cancer in the context of T2DM and dynamically observe the influence of hyperglycemia on the growth of pancreatic cancer cells in vivo， thereby providing a new experimental vector for the in vivo study of the development and progression of pancreatic cancer in the context of T2DM.

This study explored the ideas and methods of acupuncture for Guillain-Barré Syndrome （GBS） with the core principle of “to treat flaccidity， select the yangming （阳明） channel only”. The main pathological mechanism of GBS is deficiency of qi and blood in the yangming channel， malnutrition of all sinews， diminished spleen and stomach function leading to the production of pathogenic damp-heat qi， which obstructs the meridians， and gradually affects the liver and kidneys， consuming essence and damaging blood. Concurrently， dysfunction of the dumai （督脉） pivotal mechanism and lack of moisture in sinews and vessels result in symptoms such as skin numbness， paralysis， and muscle wastage. In clinical diagnosis and treatment， a combination of syndrome and channel differentiation is taken. Treatment primarily focuses on acupoints of yangming channel， aiming to supplement qi and blood， and acupoints of du mai are combined to open the vessel and fill the marrow. Specific acupoints are selected based on syndrome differentiation， providing comprehensive regulation to promote harmonization of qi and blood， relieve meridians， and the smooth generation and circulation of whole body fluids. This， in turn， enhances the strength of muscles and bones， and fosters a robust and freely moving body.