Heart failure （HF） is the end-stage of various cardiovascular diseases， with high morbidity and mortality. The existing “new quadruple” standard treatment can hardly reverse the core pathological process of myocardial remodeling， and long-term medication may pose risks of drug resistance and adverse reactions. Therefore， new therapeutic targets and strategies are urgently needed. Metabolic reprogramming is the upstream core mechanism regulating phenotypic polarization and functional activation of macrophages， which drives the occurrence and development of HF through the core axis of metabolic reprogramming-immune imbalance-ventricular remodeling and has become a cutting-edge potential target for the prevention and treatment of HF. Traditional Chinese medicine （TCM） has a long history in the prevention and treatment of HF. A large number of studies in recent years have confirmed that different therapeutic methods of TCM can correct the polarization imbalance， restore the homeostasis of myocardial immune microenvironment， inhibit myocardial injury， and delay the pathological process of HF by targeting and regulating the metabolic reprogramming of glucose， lipids， mitochondria， and amino acids in macrophages. This paper systematically expounds the core pathological mechanism of metabolic reprogramming of macrophages in HF， sorts out the research progress of TCM in preventing and treating HF by intervening this target， analyzes the regulatory rules， summarizes the limitations of existing research， and puts forward future directions. This review aims to provide a systematic theoretical reference and new research ideas for TCM clinical diagnosis and treatment and new drug development of HF.

Objective:To assess the efficacy of "three-step" strategy for preparing autologous pedicled nasal mucosal flaps in repairing cerebrospinal fluid（CSF） leaks following transsphenoidal pituitary adenoma surgery. Methods:A retrospective study was conducted on the clinical data of 25 patients who developed CSF leaks after transsphenoidal pituitary adenoma surgery at the First Affiliated Hospital of Kunming Medical University between July 2012 and June 2022. Surgical repair was selected step by step using nasal septal mucosal flap with either the posterior septal artery or septal branch of the sphenopalatine artery as the pedicle, or a pedicled middle turbinate mucosal flap. All patients underwent ≥2-year endoscopic follow-up to assess flap viability and CSF leak recurrence. Results:The median postoperative hospital stay was 4 days. Five patients developed intracranial infections postoperatively. The follow-up period ranged from 2 to 12 years. Nasal endoscopic examinations showed good mucosal flap growth, with no recurrence of CSF leakage in any of the patients. Conclusion:High-flow cerebrospinal fluid（CSF） leaks following pituitary tumor surgery pose significant challenges for clinical repair. Based on intraoperative nasal septal mucosal preservation and the condition of sellar base CSF leakage, the "three-step" strategy for preparing autologous pedicled nasal mucosal flaps-utilizing posterior septal artery, ethmoidal artery-based, or pedicled middle turbinate mucosal flaps sequentially-is a safe and effective repair method.
Humans ; Retrospective Studies ; Pituitary Neoplasms/surgery* ; Surgical Flaps ; Nasal Mucosa/surgery* ; Cerebrospinal Fluid Leak/surgery* ; Adenoma/surgery* ; Postoperative Complications/surgery* ; Male ; Female ; Middle Aged ; Adult ; Aged

The occurrence and development of atherosclerotic cardiovascular diseases is closely related to abnormally elevated plasma low density lipoprotein cholesterol(LDLC)level.Low density lipoprotein receptor(LDLR)plays a central role in the maintenance of cholesterol homeostasis by mediating the endocytotic clearance of LDLC,and the abundance of LDLR on the surface of the cell membrane is closely related to the expression level and recirculation of LD-LR.Recent studies have found that RING-E3 ubiquitin ligase can regulate LDLR levels through a dual mechanism:on the one hand,it directly ubiquitinates and modifies LDLR to promote its degradation via the endosome-lysosome pathway;on the other hand,it reduces LDLR synthesis through activation of the liver X receptor(LXR)pathway or inhibition of the nuclear translocation of sterol regulatory element-binding protein(SREBP).Together,these two mechanisms lead to a decrease in cell membrane LDLR abundance,impairing cholesterol metabolic homeostasis and exacerbating LDLC accumu-lation.Therefore,targeted inhibition of RING-E3 ubiquitin ligase activity may be a novel strategy to regulate LDLR ex-pression,reduce plasma LDLC levels,and combat cardiovascular disease.This article reviews the mechanism of action of RING-E3 ubiquitin ligase in regulating LDLR and its related research progress.

The occurrence and development of atherosclerotic cardiovascular diseases is closely related to abnormally elevated plasma low density lipoprotein cholesterol(LDLC)level.Low density lipoprotein receptor(LDLR)plays a central role in the maintenance of cholesterol homeostasis by mediating the endocytotic clearance of LDLC,and the abundance of LDLR on the surface of the cell membrane is closely related to the expression level and recirculation of LD-LR.Recent studies have found that RING-E3 ubiquitin ligase can regulate LDLR levels through a dual mechanism:on the one hand,it directly ubiquitinates and modifies LDLR to promote its degradation via the endosome-lysosome pathway;on the other hand,it reduces LDLR synthesis through activation of the liver X receptor(LXR)pathway or inhibition of the nuclear translocation of sterol regulatory element-binding protein(SREBP).Together,these two mechanisms lead to a decrease in cell membrane LDLR abundance,impairing cholesterol metabolic homeostasis and exacerbating LDLC accumu-lation.Therefore,targeted inhibition of RING-E3 ubiquitin ligase activity may be a novel strategy to regulate LDLR ex-pression,reduce plasma LDLC levels,and combat cardiovascular disease.This article reviews the mechanism of action of RING-E3 ubiquitin ligase in regulating LDLR and its related research progress.

Objective To explore the role and mechanism of crocin in pituitary adenoma(PA)through clinical samples and related molecular biology experiments of HP75 cells.Methods From June 2022 to May 2023,16 PA samples were collected from the Second Department of Neurology and Otolaryngology skull base surgery of the First Affiliated Hospital of Kunming Medical University.Three normal control samples were from the human anatomy of the Forensic College of Kunming Medical University.The expression of IRF7 mRNA in clinical samples was detected,and the proliferation,migration,invasion and apoptosis of HP75 cells were detected by knocking down the expression of IRF7;the expression of NF-κB was regulated by IRF7 in HP75 cells,and crocin regulated the growth of PA cells and its regulatory effect on IRF7/NF-κB signaling pathway.Results RT-qPCR and immunohisto-chemistry showed that compared with the normal control group,the expression of IRF7 mRNA in PA was significantly increased(P＜0.001);the expression of IRF7 protein in si-IRF7 group was significantly decreased(P＜0.001);CCK-8,Transwell and flow cytometry results showed that compared with the control group,knockdown of IRF7 significantly decreased the cell viability of HP75 cells(P＜0.001),inhibited the migration and invasion(P＜0.001),and promoted the apoptosis of HP75 cells(P＜0.001).In addition,knockdown of IRF7 could inhibit the expression of p-NF-κB p65/NF-κB p65(P＜0.001)and p-NF-κB p65/NF-κB p65(P＜0.001).Overexpression of IRF7 partially reversed the effect of crocin(P＜0.001)and restored the expression of p-NF-κB p65/NF-κB p65(P＜0.01).Finally,the biological behavior of HP75 cells showed that compared with crocin group,overexpression of IRF7 could improve the cell viability of HP75 cells,promote their migration and invasion,and inhibit cell apoptosis(P＜0.001).Conclusion Crocin treatment can inhibit the proliferation,migration and invasion of PA cells,promote cell apoptosis,and alleviate the development of PA.In the mechanism,IRF7 is significantly overexpressed in PA,and knockdown of IRF7 can inhibit the malignant growth of PA.Crocin can inhibit the proliferation,migration and invasion of PA cells,and promote apoptosis by inhibiting IRF7/NF-κB signaling pathway.

Aim To explore the effects of niacin on LDL-C uptake and metabolism in HepG2 cells,and to clarify the functions of niacin in lipid-lowering and slo-wing the atherosclerosis process,thus to provide a sci-entific basis for niacin as a lipid-lowering drug in clini-cal development.Methods Oil red O staining was used to observe HepG2 cells after lipid uptake.Enzy-matic method was used to determine the content of in-tracellular free cholesterol (FC)and total cholesterol (TC).The LDLR levels on the surface of cell mem-brane were detected by immunofluorescence flow cy-tometer.The mRNA and protein expressions of LDLR, SREBP2 and PCSK9 were analyzed by qPCR and Western blot.Results The results of oil red O staining showed that the rate of oil red O-positive cells and the number of red lipid droplets were significantly in-creased in niacin group than control group.Niacin sig-nificantly increased the levels of TC and FC in HepG2 cells(P <0.05 ).What’s more,niacin significantly upregulated the expression of LDLR and significantly downregulated the protein expression of PCSK9,while it had no effect on the expression of SREBP2.Conclu-sion Niacin accelerates LDL-C uptake probably via downregulating the expression of PCSK9 and reducing the degradation of LDLR protein in HepG2 cells.

Aim To explore the lipid-lowering mecha-nisms of curcumin from the molecular levels and pro-vide scientific basis for clinical development of lipid-lowering drugs.Methods Using oil red O staining and enzymic to determinate the levels of cholesterol in HepG2 cells.Moreover,uptaking of DiI-LDL was also measured.The expressions of mRNA and protein were detected by RT-Q-PCR and Western blot.Results The red lipid droplets and the levels of TC and FC sig-nificantly increased in HepG2 cells after treated with curcumin.The orange red fluorescence was higher than that of control.Curcumin could promote the expression levels of mRNA and protein of SREBP2 and LDLR, what′s more,curcumin could reduce the expression of the mature PCSK9 level and IDOL protein.Conclu-sion Curcumin accelerates LDL-C uptake probably via downregulating the expression of PCSK9 and IDOL in HepG2 cells.

Objective To study the effects of tetrahydroxy stilbene glucoside(TSG)on H2O2‐induced apoptosis of human umbilical vein endothelial cells (HUVECs)and on the expressions of X‐linked inhibitor of apoptosis protein (XIAP)and p53.Methods HUVECs were cultured in vitro and divided into 6 groups:control group ,300 μmol/L H2O2 group ,1 μmol/L TSG+ 300 μmol/L H2O2 group ,10 μmol/L TSG+300 μmol/L H2O2 group ,100 μmol/L TSG+ 300 μmol/L H2O2 group ,30μmol/L Embelin+ 10 μmol/L TSG+ 300 μmol/L H2O2 group.The morphology of apoptotic cells was observed by Hoechst 33258 staining.The mRNA and protein expressions of XIAP ,p53 ,Caspase‐3 were detected by RT‐PCR and Western blotting , respectively.Results The number of apoptotic cells and the expression level of p53 were significantly increased while the ex‐pression level of XIAP was dramatically decreased in H2O2 group as compared with control group.The expression level of p53 and the number of apoptotic cells were down‐regulated while the expression level of XIAP was up‐regulated after treatment with 10 or 100 μmol/L TSG when compared with H2O2group.Moreover ,compared with those in 10 μmol/L TSGgroup ,the number of apoptotic cells and the expression of Caspase‐3 were significantly enhanced after pretreatment with 30 μmol/L Embelin for 6 h.Conclusion TSG can inhibit H2O2‐induced apoptosis of HUVECs by down‐regulating the expression level of p53 and up‐reg‐ulating the expression level of XIAP.

AIM:To investigate high-density lipoprotein ( HDL) subclass distribution and to analyze the rela-tionship between HDL subclasses with plasma glucose and lipids in metabolic syndrome ( MS) .METHODS:Apolipopro-tein A-I ( apoA-I) contents of plasma HDL subclasses were determined by two-dimensional gel electrophoresis associated with immunodetection .The concentrations of lipids and apolipoproteins in the plasma were measured by an automated bio -chemical analyzer .RESULTS:Compared with the controls , the levels of fasting plasma glucose ( FPG) , total cholesterol (TC), triglyceride ( TG), low-density lipoprotein cholesterol ( LDL-C), LDL-C/high-density lipoprotein cholesterol (HDL-C), apolipoprotein B100(apoB100), apoB100/apoA-I, systolic blood pressure (SBP), body mass index (BMI) and HDL3b were increased in the MS patients (P<0.05).Meanwhile, HDL-C, apoA-I and preβ2-HDL, HDL2a and HDL2b were decreased in the MS patients (P<0.01).With the increase in the plasma glucose level , the contents of HDL2a and HDL2b were decreased in the MS patients (P<0.05), while preβ1-HDL was increased (P<0.05).With the decrease in the HDL-C level, the content of HDL2b was decreased in the MS patients (P<0.01), while preβ1-HDL was increased (P<0.01).With the increase in the TG level and the decrease in the HDL-C level, the content of HDL2b had a decrea-sing trend and the content of small-particle preβ1-HDL had an increasing trend , indicating that HDL maturation metabolism was disrupted.The correlation analysis showed that FPG was negatively correlated with the levels of HDL 2a and HDL2b, HDL-C was negatively correlated with the level of preβ1-HDL and positively correlated with the level of HDL 2b , and TG was positively correlated with the levels of preβ1-HDL and HDL3b .CONCLUSION:With the increases in the plasma glucose and TG, and the decrease in HDL-C in the MS patients, HDL particles have minifying tendency , and the maturation me-tabolism of HDL particles is disrupted .

According to the educational objectives of biotechnology in local universities, the fundamental ideas about reforming the experimental teaching in biotechnology were discussed from the multiple aspects including the resetting of experimental curses system , the contents and methods of teaching and the approaches of examining and assessing. The final aim is to train out more innovative biotechnological talents through systematic and standardized practice of innovative teaching to meet the needs of China during this economical and societal development.