AIM : To observe the effects of naoyikang on the capability of learning and memory in Alzheimer’s disease model mice. METHODS : The mice model was established by intraperitoneal injection of D BZ Gal and NaNO 2, the capability of learning and memory was tested on mice by electrical maze and water maze, the levels of superoxide dismutase (SOD) and malondialdehyde(MDA) of brain tissues were assayed by biochemical methods,and the changes in ultrastructure were observed by Transmission Electron Microscope. RESULTS : The capability of learning and memory of model mice decreased and the level of SOD of model mice decreased and MDA increased. Compared with the madel group, they were obviously improved in low, middle and high doses ( 2.4 , 7.2 , 24 g?kg -1 ?d -1 ) of naoyikang group ([WTBX P

AIM: To observe the protective effect of naoyikang-containing serum on cultured hippocampus neuron injury induced by D-galactose(D-gal).METHODS: Naoyikang-containing serum was prepared in rats administered with aqueous extract of naoyikang(6.84 g?kg-1?d-1).MTT,MAO-B and ATPase assay were used to measure the viability of hippocampus neurons.RESULTS: D-gal at concentration of 100 ?mol/L caused significant decrease in the viability of hippocampus neurons 24 h after the treatment.Naoyikang-containing serum increased the viability,ATPase activity and the expression of bcl-xl mRNA,decreased the MAO-B activity and the expression of bax mRNA in D-gal injured hippocampus neurons.CONCLUSION: Naoyikang-containing serum prevents hippocampus neurons from D-gal induced cytotoxicity.

Objective To analys hyperinsulinemia in Bartter syndrome. Methods Twenty-three cases of Bartter syndrome [age (27 ±9) years;fasting serum potassium(2. 8 ±0. 5)mmol/L], 20 patients of aldosterone-producing adenoma [APA, age (45 ± 11 ) years, fasting serum potassium ( 3.0 ± 0. 4 ) mmol/L], 20 patients of idiopathic hyperaldosteronism [IHA, age (51 ± 11 ) years, fasting serum potassium (3.4 ±0. 2)mmol/L] were diagnosed in Peking Union Medical College Hospital from September 2003 to May 2008. All patients underwent 3-hours oral glucose tolerance test(3hOGTT), postural stimulation test and calculated HOMA-insulin resistance ( HOMA-IR ) and HOMA-insulin sensitivity ( HOMA-IS ) by Homeostasis model.Results The insulin area under curve-(229.0±162.4)mIU·L-1·h] was singnificantly higher than APA group [(227.7±158.6)mIU·-1·h].But HOMA-IR in Bartter group were similar to APA group( 1.96 ± 1.14 vs 1.41 ± 0. 91 ), and HOMA-IR in APA group was lower than IHA group ( 1.96 ± 1.14 vs 2.40 ± 1.60, P ＜ 0. 05 ). There was no deference in HOMA-IS among three groups,but APA group had lower level. In all three groups, the peak of insulin secretion was delayed. Conclusion Bartter syndrome patients commonly present with hyperinsulinemia.

Acute liver failure is a serious and complex liver disease with a high short-term mortality rate. Its pathogenesis remains unknown and there is still a lack of effective drugs. Animal models play an important role in further revealing the pathogenesis of acute liver failure and the therapeutic mechanism of drugs, and the selection of experimental animals and preparation methods is the key to the effective implementation of research. This article summarizes the commonly used and new animal models of acute liver failure in recent years and the corresponding preparation methods and divides the animal models of acute liver failure into following four categories: chemical drug model, surgical model, infection model, and other models. Meanwhile, the above models are evaluated based on Terblanche and Hickman evaluation criteria for liver failure models, hoping to provide a reference for model selection and evaluation in basic research on this disease.

The fungus Trichophyton schoenleinii (T. schoenleinii) is the causative agent of Trichophytosis and Tinea favosa of the scalp in certain regions of Eurasia and Africa. Human innate immune system plays an important role in combating with various pathogens including fungi. The inflammasome is one of the most critical arms of host innate immunity, which is a protein complex controlling maturation of IL-1β. To clarify whether T. schoenleinii is able to activate the inflammasome, we analyzed human monocytic cell line THP-1 for IL-1β production upon infection with T. schoenleinii strain isolated from Tinea favosa patients, and rapid IL-1β secretion from THP-1 cells was observed. Moreover, applying competitive inhibitors and gene specific silencing with shRNA, we found that T. schoenleinii induced IL-1β secretion, ASC pyroptosome formation as well as caspase-1 activation were all dependent on NLRP3. Cathepsin B activity, ROS production and K⁺ efflux were required for the inflammasome activation by T. schoenleinii. Our data thus reveal that the NLRP3 inflammasome plays an important role in host defense against T. schoenleinii, and suggest that manipulating NLRP3 signaling can be a novel approach for control of diseases caused by T. schoenleinii infection.
Animals ; Bone Marrow Cells ; cytology ; Carrier Proteins ; metabolism ; Caspase 1 ; metabolism ; Cell Line ; Dendritic Cells ; cytology ; metabolism ; microbiology ; Enzyme Activation ; Hot Temperature ; Humans ; Inflammasomes ; metabolism ; Interleukin-1beta ; biosynthesis ; metabolism ; Lysosomes ; metabolism ; Mice ; Monocytes ; cytology ; metabolism ; microbiology ; NLR Family, Pyrin Domain-Containing 3 Protein ; Potassium ; metabolism ; Reactive Oxygen Species ; metabolism ; Signal Transduction ; Trichophyton ; physiology

With the optimization of surgical technologies and postoperative management regimens, the number of lung transplantation has been significantly increased, which has become an important treatment for patients with end-stage lung disease. However, due to the impact of comprehensive factors, such as bronchial ischemia and immunosuppression, the incidence of airway stenosis after lung transplantation is relatively high, which severely affects postoperative survival and quality of life of lung transplant recipients. In recent years, with the improvement of perioperative management, organ preservation and surgical technologies, the incidence of airway stenosis after lung transplantation has been declined, but it remains at a high level. Early diagnosis and timely intervention play a significant role in enhancing clinical prognosis of patients with airway stenosis. In this article, the general conditions, diagnosis, treatment and prevention of airway stenosis after lung transplantation were reviewed, aiming to provide reference for comprehensive management of airway stenosis after lung transplantation and improving clinical prognosis of lung transplant recipients.

Objective:To investigate the regulatory effect of transient receptor potential cation channel subfamily C member 3 (TRPC3) on the retina in oxygen-induced retinopathy (OIR) mice and biological behavior of human retinal vascular endothelial cells (HREC).Methods:A total of 32 healthy SPF grade 7-day-old C57BL/6 mice were selected and randomly divided into a control group and an OIR group by the random number table method, with 16 mice in each group.The control group received no special treatment, and the OIR model was established in the OIR group.On postnatal day 17 (PN17), the success of the model establishment was verified by immunofluorescence staining of the retinal patch.The in vitro cultured HREC were divided into a normal control group, a transfection reagent group, and a si-TRPC3 group.The normal control group received no special treatment, while the transfection reagent group and the si-TRPC3 group were transfected with transfection reagent or transfection reagent + si-TRPC3.The relative expression of TRPC3 mRNA was detected by real-time quantitative fluorescence PCR.The relative expressions of TRPC3, transcription factor NF-E2 related factor (Nrf2), and superoxide dismutase (SOD) proteins were determined by Western blot.HREC were further divided into a normal control group, a vascular endothelial growth factor (VEGF) group, a si-TRPC3 group, and a Pyr3 (TRPC3 channel inhibitor) group, which were cultured in complete medium, medium containing 20 ng/ml VEGF recombinant protein, medium containing 20 ng/ml VEGF recombinant protein (si-TRPC3 transfection for 72 hours), and medium containing 20 ng/ml VEGF recombinant protein+ 1 μmol/L Pyr3 for 48 hours, respectively.The proliferation ability of HREC was detected using cell counting kit 8 (CCK-8). The horizontal and vertical migration ability of cells were detected by cell scratch assay and transwell assay, respectively.This study followed the 3R principles of animal welfare and was approved by the Ethics Committee of Hebei Eye Hospital (No.2023LW04). Results:Pathological neovascular clusters with strong fluorescent staining appeared in the retina of OIR mice on PN17.The relative expressions of TRPC3 mRNA and protein in the retina of OIR mice were 2.057±0.244 and 1.517±0.290, respectively, significantly higher than 0.983±0.033 and 0.874±0.052 of control group ( t=6.165, 3.094; both at P<0.05). The relative expression levels of TRPC3 mRNA and protein were significantly lower, and the relative expression levels of Nrf2 and SOD proteins were higher in the si-TRPC3 group than in the normal control and transfection reagent groups, and the differences were statistically significant (all at P<0.05). The CCK-8 experiment results showed that the cell absorbance value was higher in the VEGF group than in the normal control group, and lower in the si-TRPC3 and Pyr3 groups than in the VEGF group, with statistically significant differences (all at P<0.05). The results of the cell scratch experiment showed that the lateral migration rate of VEGF group cells was higher than that of normal control group, while the lateral migration rate of si-TRPC3 group and Pyr3 group cells was lower than that of VEGF group, and the differences were statistically significant (all at P<0.05). The transwell experiment results showed that the number of stained cells in the VEGF group was higher than that in the normal control group, and the number of stained cells in the si-TRPC3 group and Pyr3 group was lower than that in the VEGF group, with statistically significant differences (all at P<0.05). Conclusions:Hypoxia induces increased TRPC3 expression in OIR mouse retina, and downregulation of TRPC3 inhibits HREC proliferation and migration.The mechanism is related to the activation of the Nrf2-related oxidative stress pathway.

Liver failure is a common end-stage liver disease syndrome in clinical practice characterized by massive necrosis of hepatocytes leading to rapid liver failure, and it is currently believed that excessive inflammation and immune response are the core mechanisms of this disease. Endogenous lipid mediators are involved in the regulation of a variety of inflammatory processes, including initiation, maintenance, and regression, and eicosanoids and pro-decomposition lipid mediators, as well as their complex metabolic pathways and transduction signals, play a key role in the regulation of these processes. This article reviews the key role of endogenous lipid mediators in the pathophysiological mechanism of inflammation and immune dysfunction in liver failure and the potential significance and new therapeutic opportunities of lipid immune pathway in liver failure, in order to provide new ideas for the clinical diagnosis and treatment of liver failure.

Glycolysis plays an important role in the development and progression of liver diseases and shows varying degrees of enhancement in different liver diseases, and it is closely associated with mitochondrial dysfunction (oxidative phosphorylation deficiency and reactive oxygen species production), which helps to fill energy production deficiency caused by impaired oxidative phosphorylation. Therefore, it might be possible to search for potential new therapies for liver diseases through targeted regulation of the key factors in aerobic glycolysis, such as hexokinase 2, pyruvate kinase M2, and other regulatory pathways. From the perspective of the association between glycolysis and liver diseases, this article elaborates on the therapeutic significance and potential value of glycolysis in liver diseases, in order to provide new ideas for the diagnosis and treatment of liver diseases.

Inflammation is closely associated with the development of cancer. Tumor-associated macrophages (TAM) actively participate in tumor-related inflammation and promote tumor growth and metastasis, while under certain conditions, TAM also show cytotoxicity and tumor killing activity and thus inhibit the progression of cancer. Crosstalk between TAM and neighboring cells is closely associated with the progression of hepatocellular carcinoma (HCC) and drug resistance during treatment. This article summarizes the role of macrophages in HCC and the crosstalk between macrophages and other cells, so as to provide new strategies for the clinical diagnosis and treatment of HCC.