ObjectiveThis paper aims to observe the role of Danlou tablet in treating coronary heart disease （CHD） with phlegm-stasis intermingling syndrome in minipigs by improving platelet function and explore the potential pharmacological mechanism of Danlou tablet in regulating platelet function by using proteomics technology. MethodsThirty Bama minipigs were randomly divided into a normal control group （6 pigs） and a high-fat diet group （24 pigs）. After 2 weeks of high-fat diet feeding， the high-fat diet group was randomly subdivided into a model group， an atorvastatin group （1 mg·kg^-1）， and Danlou tablet groups （0.6 g·kg^-1 and 0.3 g·kg^-1）. All groups continued to receive a high-fat diet for 8 weeks after the procedure. The normal control group was given a regular diet， underwent only coronary angiography， and did not receive an interventional injury procedure. The model group and each administration group were fed a high-fat diet. Two weeks later， they underwent a coronary angiography injury procedure. After the procedure， drugs were mixed into the feed every morning for 8 consecutive weeks， with the minipigs maintained on a continuous high-fat diet during this period. Quantitative proteomics technology was further used to study platelet proteins， and differential proteins were obtained by screening. Bioinformatics analysis was performed to analyze key regulatory proteins and biological pathways involved in the therapeutic effect of Danlou tablet on CHD with phlegm-stasis intermingling syndrome. ResultsCompared with the normal control group， the model group showed a significant increase in total cholesterol （TC）， triglyceride （TG）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） of minipigs' serum （P<0.01）， a significant shortening in prothrombin time of （PT） （P<0.01）， a coagulation function index， and an increase in whole blood viscosity （P<0.01） and platelet aggregation rate （P<0.01）. Moreover， the platelet morphology was altered， and the contents of endothelin-1 （ET-1） and nitric oxide （NO） were significantly increased （P<0.01）. Hemodynamic parameters were obviously abnormal， including significantly decreased systolic blood pressure （SBP）， diastolic blood pressure （DBP）， mean arterial pressure （MAP）， left ventricular systolic pressure （LVSP）， and left ventricular maximal positive dp/dt （LV+dp/dt_max） （P<0.01）. Left ventricular maximal negative dp/dt （LV-dp/dt_max） was significantly increased （P<0.01）. Besides， there were myocardial cell hypertrophy， obvious edematous degeneration， massive interstitial inflammatory cell infiltration， high degree of fibrosis， and coronary endothelial atherosclerosis. TC and TG levels in minipigs' serum were significantly reduced in Danlou tablet groups with 0.6 g·kg^-1 and 0.3 g·kg^-1 （P<0.05， P<0.01）， compared with those in the model group. LDL-C was decreased in the Danlou tablet group with 0.6 g·kg^-1 （P<0.05）. The whole blood viscosity under low and high shear conditions was significantly reduced in the Danlou tablet group with 0.6 g·kg^-1 （P<0.05）. In groups with all doses of Danlou tablet， maximum aggregation rate （MAR） and average aggregation rate （AAR） were significantly decreased （P<0.05， P<0.01）， and platelets' morphological changes such as pseudopodia extension were reduced. ET-1 levels in the serum were significantly reduced. In the Danlou tablet group with 0.6 g·kg^-1， NO level in the serum was reduced （P<0.05）. In groups with all doses of Danlou tablet， DBP and MAP were significantly increased （P<0.05）. In the Danlou tablet group with 0.6 g·kg^-1， LVSP and LV+dp/dt_max were significantly increased （P<0.05， P<0.01）， and LV-dp/dt_max was significantly decreased （P<0.05）. In groups with all doses of Danlou tablet， edematous degeneration in myocardial tissue was milder， and coronary artery lesion degree was significantly alleviated. Compared with the normal control group， there were 94 differentially expressed proteins in the model group， including 81 up-regulated and 13 down-regulated proteins. Compared with the model group， the Danlou tablet group with 0.6 g·kg^-1 showed 174 differentially expressed proteins， including 100 up-regulated and 74 down-regulated proteins. A total of 30 proteins were reversed after Danlou tablet intervention. Bioinformatics analysis revealed that its pharmacological mechanism may exert anti-platelet activation， aggregation， and adhesion effects through biological pathways such as regulation of actin cytoskeleton， platelet activation pathway， Fcγ receptor-mediated phagocytosis， as well as proteins such as growth factor receptor-bound protein 2 （GRB2）， Ras-related C3 botulinum toxin substrate 2 （RAC2）， RAC1， and heat shock protein 90 alpha family class A member 1 （HSP90AA1）. ConclusionDanlou tablet can effectively reduce platelet activation and aggregation， exerting a good therapeutic effect on CHD with phlegm-stasis intermingling syndrome in minipigs. Its pharmacological mechanism may involve regulating biological pathways such as actin cytoskeleton and platelet activation pathway， as well as proteins like GRB2， RAC2， RAC1， and HSP90AA1， thereby exerting a pharmacological effect in anti-platelet activation， aggregation， and adhesion.

ObjectiveTaking the cuproptosis/oxidative stress pathway as the entry point， this study investigated the effect and mechanism of Liangyi Paste on hepatic lipid deposition in naturally aged mice fed with a high-fat diet. MethodsAfter adaptive feeding， 80 ten-week-old male C57BL/6 mice were used. Thirty of them were randomly divided into three groups （10 mice per group）： The 12-month-old control group （12MCON）， the 15-month-old control group （15MCON）， and the 15-month-old group with a high-fat diet （15MHFD）. The 12MCON and 15MCON groups were continuously fed a standard diet， while the 15MHFD group started receiving a high-fat diet at 12 months of age. Tissue samples were collected at the corresponding time points for each group. The remaining 50 mice were randomly divided into five groups （10 mice per group）： the 20-month-old control group （20MCON）， the model group， and the low-， medium-， and high-dose Liangyi Paste groups （2.91 ， 5.82 ， 11.64 g·kg^-1·d^-1， respectively）. The 20MCON group was continuously fed a standard diet， while the other groups started receiving a high-fat diet at 15 months of age. At 18 months of age， the Liangyi Paste groups were administered the corresponding doses of Liangyi Paste by gavage， while the 20MCON and model groups were given an equal volume of saline by gavage. After 8 weeks of continuous gavage （when the mice reached 20 months of age）， tissue samples were collected. Hepatic TG levels were measured using assay kits； liver histology and lipid deposition were observed via hematoxylin-eosin （HE） and oil red O staining； reactive oxygen species （ROS） were detected by enzyme-linked immunosorbent assay （ELISA）； Cu²⁺， superoxide dismutase （SOD）， and malondialdehyde （MDA） levels were measured by colorimetry； mRNA and protein expression of genes related to cuproptosis and oxidative stress pathways were analyzed by Real-time polymerase chain reaction（Real-time PCR） and Wes automated protein expression system. ResultsCompared with 12MCON， the 15MCON group showed significantly increased hepatic TG， Cu²⁺， ROS， and MDA levels （P<0.01）， decreased SOD （P<0.01）， hepatocyte swelling， and disordered arrangement. The mRNA and protein levels of ferredoxin 1 （FDX1）， dihydrolipoamide S-acetyltransferase （DLAT）， heat shock protein 70 （HSP70）， dihydrolipoamide dehydrogenase （DLD）， pyruvate dehydrogenase E1 subunit-β （PDHB）， nuclear factor erythroid 2-related factor 2 （Nrf2）， and peroxisome proliferator-activated receptor γ （PPARγ） were significantly elevated （P<0.05， P<0.01）. Compared with 15MCON group， the 15MHFD and 20MCON groups exhibited further increases in TG， Cu²⁺， ROS， and MDA （P<0.01）， reduced SOD （P<0.01）， and aggravated hepatocyte swelling and disorder. There were increased lipid droplets with mild vacuolization in the 15MHFD group， and no significant lipid deposition was observed in the 20MCON group. FDX1， DLAT， HSP70， DLD， PDHB， Nrf2， and PPARγ mRNA and protein levels were significantly increased （P<0.05， P<0.01）. Compared with 20MCON group， the model group demonstrated markedly elevated TG， Cu²⁺， ROS， and MDA （P<0.01）， reduced SOD （P<0.01）， severe hepatic steatosis， and upregulated expression of FDX1， DLAT， HSP70， DLD， PDHB， Nrf2， and PPARγ mRNA and proteins （P<0.05， P<0.01）. All abnormalities were significantly reversed after Liangyi Paste treatment. ConclusionLiangyi paste can ameliorate hepatic lipid deposition in naturally aged mice with a high-fat diet by modulating the cuproptosis/oxidative stress pathway.

Based on the traditional Chinese medicine （TCM） theories of body fluid metabolism and turbid phlegm obstructing the orifices， and drawing on recent advances in cerebrospinal fluid-interstitial fluid （CSF-ISF） exchange， glymphatic clearance， and extracellular matrix （ECM） regulation， this article discusses the possible scientific connotation of "invisible phlegm" from the perspectives of pathogenesis， clinical manifestations， and therapeutic implications. Impaired brain fluid exchange may lead to reduced clearance， the retention of metabolic wastes and pathological proteins. Abnormal ECM remodeling may further disrupt molecular diffusion and local microenvironmental homeostasis， resulting in a pathological process characterized by slowed fluid movement， reduced clearance， and abnormal retention. This process bears a certain functional resemblance to the TCM pathogenesis of impaired distribution of body fluids， endogenous formation of turbid phlegm and obstruction of the brain orifices， and may also be associated with manifestations such as a clouded sensation in the head， cognitive abnormalities， and emotional disturbances. On this basis， the potential effects of certain phlegm-dissolving Chinese medicines in improving brain clearance function and extracellular microenvironmental homeostasis warrant further investigation. We therefore propose that， the "invisible phlegm" of TCM in brain tissue may manifest as a pathological retention state characterized by restricted fluid exchange， impaired clearance function， and extracellular microenvironmental imbalance. This perspective may provide a new avenue for investigating TCM treatment of neurological and psychiatric disorders from the perspective of phlegm.

Based on the traditional Chinese medicine （TCM） theories of body fluid metabolism and turbid phlegm obstructing the orifices， and drawing on recent advances in cerebrospinal fluid-interstitial fluid （CSF-ISF） exchange， glymphatic clearance， and extracellular matrix （ECM） regulation， this article discusses the possible scientific connotation of "invisible phlegm" from the perspectives of pathogenesis， clinical manifestations， and therapeutic implications. Impaired brain fluid exchange may lead to reduced clearance， the retention of metabolic wastes and pathological proteins. Abnormal ECM remodeling may further disrupt molecular diffusion and local microenvironmental homeostasis， resulting in a pathological process characterized by slowed fluid movement， reduced clearance， and abnormal retention. This process bears a certain functional resemblance to the TCM pathogenesis of impaired distribution of body fluids， endogenous formation of turbid phlegm and obstruction of the brain orifices， and may also be associated with manifestations such as a clouded sensation in the head， cognitive abnormalities， and emotional disturbances. On this basis， the potential effects of certain phlegm-dissolving Chinese medicines in improving brain clearance function and extracellular microenvironmental homeostasis warrant further investigation. We therefore propose that， the "invisible phlegm" of TCM in brain tissue may manifest as a pathological retention state characterized by restricted fluid exchange， impaired clearance function， and extracellular microenvironmental imbalance. This perspective may provide a new avenue for investigating TCM treatment of neurological and psychiatric disorders from the perspective of phlegm.

Specification for Quality Control in Traditional Chinese Medicine Clinical Trials（GB/T 47336-2026） is the first national standard in the field of clinical research on traditional Chinese medicine （TCM）， aims to address the core issue that the quality shortcomings of current TCM clinical research restrict the transformation of achievements and international recognition. Through the interpretation of the core contents of this standard， including its scope of application， graded quality control system， TCM-specific quality control requirements， implementation and responsible entities， responsibilities of quality control personnel， formulation of quality control plans， critical nodes of quality control， and quality control archive management， it is believed that the promotion and implementation of this standard are of great significance for improving the standard system of TCM clinical research， enhancing research quality， optimizing the quality management model， and promoting the internationalization process of TCM. Meanwhile， the implementation paths for the standard are discussed， including carrying out pilot applications in institutions， establishing publicity， implementation， and training mechanisms， encouraging multi-party collaborative supervision， and setting up implementation feedback mechanisms. On this basis， the challenges that may be encountered during implementation， such as resource input pressure， difficulties in implementing TCM-specific quality control， and a relative shortage of interdisciplinary composite talents， are sorted out， and corresponding strategies are proposed， which can provide references for relevant researchers and practitioners.

ObjectiveTo investigate the intervention effect of modified Xiangsha Liujunzitang （M-XSLJZ） on insulin resistance-regulated fatty acid synthesis via Lon protease 1 （Lonp1） in the liver of spleen-deficiency hyperlipidemia rats. MethodsA total of 70 male SD rats were randomly allocated into seven groups （n=10）： blank control group， high-fat diet （HFD） group， spleen-deficiency hyperlipidemia （PX-HFD） model group， low-， medium-， and high-dose Modified Xiangsha Liujunzitang （JW-L， JW-M， JW-H）， and rosuvastatin group. The spleen-deficiency model was induced in the PX-HFD， JW-L， JW-M， JW-H， and rosuvastatin groups by irregular diet combined with exhaustive swimming. Except for the control group， all groups were fed an HFD for 10 weeks to establish a hyperlipidemia rat model. Following modeling， the rats in the JW-L， JW-M， and JW-H groups received the decoction by gavage at 3.51， 7.02， 14.04 g·kg^-1， respectively， while the rosuvastatin group received 9×10^-4 g·kg^-1. After 8 weeks of administration， samples were collected. D-xylose excretion rate was quantified using the phloroglucinol method. Serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） were measured by an automatic biochemical analyzer. Hepatic TG content was quantified by the glycerol phosphate oxidase-peroxidase anti-peroxidase （GPO-PAP） method. Serum insulin （INS）， fasting blood glucose （FBG）， hepatic reactive oxygen species （ROS） levels， and mitochondrial complex Ⅰ activity were assessed by enzyme-linked immunosorbent assay （ELISA）. The mRNA levels of Lonp1， and acetyl-CoA carboxylase 1 （ACC1） were determined by real-time quantitative PCR （Real-time PCR）. Protein expression levels of Lonp1， c-Jun N-terminal kinase （JNK）， phosphorylated （p）-JNK， insulin receptor substrate 1 （IRS1）， p-IRS1， and ACC1 in liver tissues were analyzed by Western blot. ResultsCompared with the control group， the HFD group showed a significant increase in body weight （P<0.01）. The PX-HFD group showed a significant decrease in D-xylose excretion rate （P<0.01）. Both the HFD and PX-HFD groups exhibited significantly elevated serum levels of TC， TG， HDL-C， LDL-C， FBG， INS， and HOMA-IR （P<0.01）， along with increased orange-red lipid droplets， prominent fatty vacuoles， and significantly elevated hepatic TG level （P<0.01）. Mitochondrial complex Ⅰ activity significantly decreased （P<0.05）， while ROS level， Lonp1 mRNA and protein expression， and ACC1 mRNA and protein expression significantly increased （P<0.05， P<0.01）. The p-IRS1/IRS1 protein expression ratio significantly decreased （P<0.01）， whereas the p-JNK/JNK protein expression ratio significantly increased （P<0.01）. Compared with the HFD group， the PX-HFD group showed significantly reduced D-xylose excretion rate and serum HDL-C level （P<0.01）， significantly decreased hepatic TG level （P<0.05）， and significantly increased HOMA‑IR index （P<0.01）. Hepatic Lonp1 mRNA and protein expression significantly decreased （P<0.05， P<0.01）， p‑IRS1/IRS1 protein expression ratio was significantly decreased （P<0.01）， while ACC1 mRNA and protein expression and p‑JNK/JNK protein expression ratio were significantly increased （P<0.01）. Compared with the PX-HFD group， all treatment groups showed significantly reduced serum TC， TG， LDL-C levels， and HOMA-IR index （P<0.05， P<0.01）， with ameliorated orange‑red lipid droplet deposition and significantly reduced hepatic TG and ROS levels （P<0.05， P<0.01）. The JW-M， JW-H， and rosuvastatin groups exhibited significantly decreased body weight （P<0.05， P<0.01）， significantly increased D‑xylose excretion rate （P<0.01）， significantly decreased HDL‑C level （P<0.05， P<0.01）， significantly increased mitochondrial complex I activity， Lonp1 mRNA and protein expression， and p-IRS1/IRS1 protein expression ratio （P<0.05， P<0.01）， as well as significantly decreased p-JNK/JNK protein expression ratio （P<0.01）. ConclusionM-XSLJZ may exert its lipid‑lowering effect by regulating Lonp1 expression in rat liver， thereby improving insulin resistance and subsequently inhibiting hepatic lipid synthesis.

ObjectiveTo investigate the regulatory effect of icariin （ICA） on transforming growth factor-β₁ （TGF-β₁）/Smad pathway in bone microvascular endothelial cells （BMECs） and the effect on autophagy in BMECs. MethodsBMECs were isolated and cultured， and the cell types were identified by immunofluorescence. Cells were divided into the control group， model group （0.1 g·L^-1 methyl prednisolone）， ICA group （0.1 g·L^-1 methyl prednisolone +1×10^-5 mol·L^-1 ICA）， and TGF-β inhibitor group （0.1 g·L^-1 methyl prednisolone +1×10^-5 mol·L^-1 ICA +1×10^-5 mol·L^-1 LY2157299）. Transmission electron microscopy was used to observe the ultrastructure and autophagosome number of BMECs. Autophagy double-standard adenovirus was used to monitor the confocal autophagy flow generation of each cell. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to detect the gene and protein expression of autophagy in the TGF-β₁/ Smad pathway. ResultsAfter cell separation culture， platelet endothelial cell adhesion molecule （CD31） and von willebrand factor （vWF） immunofluorescence identified BMECs. Transmission electron microscopy showed that the cell membrane was damaged， and the nucleus was pyknotic and broken in the model group. Compared with the model group， the ICA group had complete cell membranes， clear structures， with autophagy-lysosome sparsely distributed. The confocal photo showed that BMECs had autophagosomes and autophagy-lysosomes， and the autophagy expression of the ICA group was similar to that of the blank group. Compared with the blank group， in the model group and the LY2157299 group， autophagosomes and autophagy-lysosomes were barely seen in the autophagy flow. Compared with the blank group， the mRNA and protein expressions of autophagy effector protein 1 （Beclin1） and microtubule-associated protein 1 light chain 3B （LC3B） in the model group were significantly decreased （P<0.01）， and those of ubiquitin-binding protein （p62） were significantly increased （P<0.01）. The mRNA expression of TGF-β₁， Smad homolog 2 （Smad2）， and Smad homolog 3 （Smad3） decreased （P<0.05， P<0.01）. The protein expressions of TGF-β₁， p-Smad2， and p-Smad3 were significantly decreased （P<0.01）. Compared with those of the model group， the mRNA and protein expression of Beclin1 and LC3B in BMECs of the ICA group increased （P<0.01）， and those of p62 significantly reduced （P<0.01）. The mRNA expression of TGF-β₁， Smad2， and Smad3 increased significantly （P<0.01）. The protein expression of TGF-β₁， p-Smad2， and p-Smad3 increased significantly （P<0.01）. Compared with those in the model group， the mRNA and protein expressions of Beclin1， LC3B， and p62 in the inhibitor group were not statistically significant. The expression of key genes and proteins of the TGF-β₁ pathway in the inhibitor group was not statistically significant. ConclusionICA can promote glucocorticoid-induced autophagy expression of BMECs， and its mechanism may be related to activating the TGF-β₁/Smad signaling pathway.

ObjectiveThe study aims to investigate the intervention effect of modified Xiangsha Liujunzitang （M-XSLJZ） on intestinal-derived lipopolysaccharide （LPS）-activated Kupffer cell inflammation in rats with hyperlipidemia spleen deficiency syndrome. MethodsSeventy male SD rats were randomly divided into seven groups （n=10）： blank control （CON）， high-fat diet without spleen deficiency （HFD）， high-fat diet with spleen deficiency （SD-HFD）， M-XSLJZ low-， medium-， and high-dose groups （XS-L， XS-M， XS-H）， and western medicine control （R）. Spleen deficiency was induced in SD-HFD， XS-L， XS-M， XS-H， and R groups via irregular diet combined with exhaustive swimming for 15 days. The CON group received a standard diet， while other groups were fed a high-fat diet for 10 weeks to establish the hyperlipidemia model. After successful modeling， rats were treated for 8 weeks： M-XSLJZ was administered at 3.51， 7.02， 14.04 g·kg^-1 in XS-L， XS-M， and XS-H groups， respectively. The R group received 9×10^-4 g·kg^-1 of a reference drug. D-xylose excretion rate was measured by the phloroglucinol method. Blood lipids were assessed using an automated biochemical analyzer. Hematoxylin-eosin （HE） staining was used to evaluate the pathological conditions of the liver， and oil red O staining was used to observe the lipid deposition in the liver. The levels of LPS， portal vein serum LPS， LPS-binding protein （LBP）， serum interleukin-6 （IL-6）， IL-1β， and tumor necrosis factor-α （TNF-α） were detected by enzyme-linked immunosorbent assay （ELISA）. Immunofluorescence was used to evaluate CD86 expression and CD68/TLR4 co-localization in the liver. Protein levels of TLR4， MyD88， NF-κB p65， and p-NF-κB p65 in Kupffer cells were analyzed via Western blot automated protein analysis. Hepatic IL-6， TNF-α， and IL-1β mRNA and protein levels were measured using Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot. ResultsCompared with the CON group， the SD-HFD group showed a decrease in D-xylose excretion （P<0.01）. TC， TG， HDL-C， and LDL-C increased （P<0.05， P<0.01）. A large number of hepatic lipid vacuoles and orange-red lipid droplet deposition appeared in the liver. Ileal LPS， portal LPS， and LBP increased （P<0.05， P<0.01）. The levels of serum IL-6， TNF-α， and IL-1β increased （P<0.01）. The expression of CD86 was upregulated （P<0.01）， and the co-expression of CD68 and TLR4 was enhanced. The protein levels of TLR4， MyD88， and p-p65 in Kupffer cells increased （P<0.01）. The mRNA and protein levels of IL-6， TNF-α， and IL-1β increased （P<0.05， P<0.01）. Compared with the HFD group， the SD-HFD group exhibited decreased D-xylose excretion （P<0.01）， higher HDL-C， LDL-C （P<0.05）， increased portal LBP and LPS （P<0.05）， increased serum IL-6 and TNF-α （P<0.01）， upregulated CD86 （P<0.01）， enhanced CD68/TLR4 co-expression， and higher TNF-α mRNA/protein （P<0.05）. Compared with the SD-HFD group， all M-XSLJZ treatment groups showed reduced TC， TG， and LDL-C （P<0.05， P<0.01）. XS-H and R groups displayed improved hepatic lipid deposition. XS-H and R groups had lower ileal LPS， portal LPS， and LBP levels （P<0.05， P<0.01）. All M-XSLJZ treatment groups exhibited reduced serum IL-6， IL-1β， and TNF-α （P<0.01）. The XS-H group showed downregulated CD86 （P<0.01） and weakened CD68/TLR4 co-expression. The XS-H group had reduced TLR4， MyD88， and p-NF-κB p65 in Kupffer cells （P<0.01）. XS-H and R groups showed lower IL-6， TNF-α， and IL-1β mRNA/protein （P<0.05， P<0.01）. ConclusionM-XSLJZ may exert its lipid-lowering effects by inhibiting intestinal-derived LPS and alleviating Kupffer cell inflammation in the liver.

Objective Based on apolipoprotein a-Ⅰ(Apoa-Ⅰ)gene knockout mice,the role and mechanism of phosphotidylcholine(PC)in improving cholesterol reverse transport were explored.Methods Thirty Apoa-Ⅰ-/-mice were randomly divided into an Apoa-Ⅰ-/-group,Apoa-Ⅰ-/-+HFD group,and Apoa-Ⅰ-/-+HFD+PC group using the random number table method;30 C57BL/6J mice were randomly divided into a WT group,WT+HFD group,and WT+HFD+PC control groups,with 10 mice in each group.The Apoa-Ⅰ-/-group and WT groups were fed basic feed,while the other groups were fed high-fat feed for 8 weeks to establish a hyperlipidemia model.From the 9th week,the WT+HFD+PC group and Apoa-Ⅰ-/-+HFD+PC group were given PC 2.5 g/(kg·d),while the remaining mice were given physiological saline by gavage for a total of 4 weeks of intervention.The serum lipid levels of the mice were detected using a fully automated analyzer.Hematoxylin and eosin and Oil red O staining were used to observe pathological and morphological changes,and the COD-PAP method was used to detect cholesterol levels in mouse liver tissue.The ELISA method was used to detect LCTA levels in mouse serum,and RT-qPCR and Western Blot method were used to detect the mRNA and protein expression of cholesterol ATP binding cassette transporter A1(ABCA1),ATP binding cassette transporter G1(ABC A1),lecithin cholesterol acyltransferase(LCAT),hepatic lipase(HL),scavenger receptor class B type Ⅰ(SR-B1),and low-density lipoprotein receptor(LDL-R)in liver tissue.Results Compared with the WT group,the serum lipid levelsof WT+HFD group mice were significantly increased(P＜0.01),LCAT levels were significantly reduced(P＜0.05),hepatic fat vacuoles were obvious,hepatic lipid deposition was significant,and liver tissue TC levels were significantly increased(P＜0.01).The mRNA and protein expression of ABCA1,ABCG1,LCAT,SR-B1,HL,and LDL-R were significantly reduced(P＜0.05,P＜0.01).Compared with the WT+HFD group,serum lipid levels in the WT+HFD+PC group were significantly reduced(P＜0.05,P＜0.01),LCAT levels were significantly increased(P＜0.05),hepatic fat vacuoles were significantly reduced,hepatic lipid deposition was alleviated,and liver tissue TC levels were significantly reduced(P＜0.05);mRNA and protein expression of ABCA1,LCAT,SR-B1,HL and LDL-R were significantly increased(P＜0.05,P＜0.01).The serum levels of TC,TG,and LDL-C were significantly increased,while the levels of LCAT、HDL-C were significantly reduced(P＜0.05,P＜0.01)in the Apoa-Ⅰ-/-+HFD group mice.Hepatocytes underwent balloon-like transformation,liver lipid deposition was significantly aggravated,and liver tissue TC levels were significantly increased(P＜0.05).The mRNA and protein expression of ABCA1,LCAT and HL were significantly reduced(P＜0.05,P＜0.01).Compared with the WT+HFD+PC group mice,the Apoa-Ⅰ-/-+HFD+PC group mice showed a significant increase in serum lipid levels(P＜0.05,P＜0.01),LCAT levels were significantly reduced(P＜0.05),significant hepatic lipid vacuoles,significant hepatic lipid deposition,and a significant increase in TC levels in liver tissue(P＜0.05).Their mRNA and protein expression of ABCA1,ABCG1,LCAT,SR-B1,and HL were also significantly reduced(P＜0.05,P＜0.01).Conclusions Phosphatidylcholine can improve dyslipidemia by interfering with Apoa-Ⅰ and thus regulating cholesterol reverse transport.

Objective:To evaluate the clinical efficacy of proximal femoral reconstruction osteotomy (PFRO) in hip revision arthroplasty.Methods:A retrospective analysis was conducted of the 92 patients (93 hips) who had undergone PFRO in hip revision arthroplasty at Department of Orthopedics, The First Affiliated Hospital, University of Science and Technology of China from January 2019 to December 2023. The cohort included 50 males (51 hips) and 42 females (42 hips), with an age of (64.5±11.7) years and a body mass index of (23.7±2.9) kg/m 2. Surgical procedures were performed under general anesthesia via a posterolateral approach. Biologic prostheses were used in femoral reconstruction, and PFRO fragments repositioned and fixed using cerclage wires. The data collected were operative time, intraoperative blood loss, length of osteotomy fragments, healing at the osteotomy site, intraoperative and follow-up complications, as well as Harris hip score (HHS) and leg length discrepancy (LLD) at the last follow-up. Results:For this cohort, operative time was (174.9±45.6) minutes, intraoperative blood loss (594.6±206.6) mL, and length of osteotomy fragments (12.3±2.3) mm. The 92 patients were followed up for (35.8±12.3) months. For them, HHS improved from preoperative (38.3±8.5) points to (80.5±12.8) points at the last follow-up, and LLD decreased from preoperative (21.2±13.0) mm to 2.0(0.0, 5.0) mm at the last follow-up, showing significant differences ( P<0.05). The osteotomy sites healed in 89 cases (90 hips), with a displacement of the greater trochanter <5 mm; 3 cases (3 hips) experienced nonunion with wire loosening and a displacement of the greater trochanter >10 mm. The osteotomy fragment of the greater trochanter got fractured in 2 patients (2 hips) and a fracture of the medial cortex of the proximal femur occurred in 11 patients (11 hips), but follow-ups observed healing of all the fractures. One patient (1 hip) developed postoperative posterior dislocation of the hip which was treated conservatively. One patient (1 hip) developed postoperative periprosthetic infection which did not recur after twice of debridement followed by prosthetic revision of the proximal femoral tumor. Conclusion:In hip revision arthroplasty, as PFRO demonstrates a low incidence of fragment fractures of the greater trochanter and a high rate of healing at the osteotomy site, its short-term clinical outcomes are satisfactory.