ObjectiveTo construct a standardized diagnostic scale for Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease. MethodsLiterature related to Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease was retrieved from CNKI， VIP， and Wanfang databases. Diagnostic information from four diagnostic methods was extracted and standardized， with items having a frequency of ≥15 included in the item pool. A three-round Delphi expert consultation was conducted， screening items using support degree， mean score， rank sum， and coefficient of variation. Item weights were determined using analytic hierarchy process （AHP）， gactor analysis （FA）， and combined weighting method （CWM）. The optimal weighting method was selected by comparing the area under the receiver operating characteristic （ROC） curve （AUC）. The Youden index was calculated to establish the diagnostic cutoff value， which was proportionally scaled. ResultsA total of 102 studies were included. Thirty-five items were incorporated into the item pool. The authority coefficients for the three Delphi rounds were 0.82， 0.85， and 0.86， with coordination coefficients of 0.648， 0.538， and 0.506， respectively. Fifteen items were retained after screening. ROC curve analysis showed the AUC ranking as FA > CWM > AHP. The maximum Youden index was 0.814， corresponding to a diagnostic cutoff of 8.361 （scaled to 40 points）. The final scale adopted a structured diagnostic framework： the symptom dimension requires at least 2 items， and the tongue or pulse dimension requires at least 1 category. ConclusionThis study developed a standardized diagnostic scale for Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease. Core items were screened via the Delphi method， with factor analysis identified as the optimal weighting method through AUC comparison. The diagnostic threshold （40 points） and structured diagnostic framework provide a quantitatively clear， clinically practical tool.

ObjectiveTo explore the establishment of a rat model of diabetic macrovascular atherosclerosis （DMA） with Qi and Yin deficiency syndrome induced by high-fat diet， streptozotocin （STZ）， and Yin-depleting herbs， and to evaluate its biological characteristics. MethodsForty SD rats were randomly divided into a blank group （n=10） and a modeling group （n=30）. Except for the blank group， rats in the model group were fed a high-fat diet for 4 weeks， followed by intraperitoneal injection of STZ （30 mg·kg^-1） to establish a diabetic model. Twenty-four successfully modeled diabetic rats were randomly divided into a model group （n=7）， a Qi and Yin deficiency syndrome group （n=8）， and a counter-syndrome group （n=9）. Except for the model group， rats received intragastric administration of Yin-depleting herbs （1.2 g·kg^-1） for 8 weeks. The counter-syndrome group was further treated with Shenqi compound formula （1.69 g·kg^-1） for an additional 8 weeks. General condition and body weight were recorded， and syndrome-related indicators were assessed， including precordial temperature， skin moisture content， grip strength， open-field test performance， and tongue appearance. Serum levels of vascular endothelial growth factor （VEGF）， endothelin-1 （ET-1）， vascular cell adhesion molecule-1 （VCAM-1）， insulin-like growth factor-1 （IGF-1）， and monocyte chemotactic protein-1 （MCP-1） were measured by enzyme-linked immunosorbent assay （ELISA）. Fasting blood glucose， blood lipids， hemorheological parameters， and coagulation function were analyzed using an automatic biochemical analyzer. Vascular ultrasound and hematoxylin-eosin （HE） staining were used to evaluate vascular lesions. ResultsIn terms of syndrome manifestations， compared with the blank group， body weight increased rapidly during the first 5 weeks in the model， Qi and Yin deficiency， and counter-syndrome groups. After STZ injection combined with Yin-depleting herbal administration at week 5， body weight decreased significantly （P<0.01） and continued to decline until the end of the experiment. Rats exhibited decreased activity， irritability， coarse and yellowish fur with obvious shedding， polydipsia， polyphagia， frequent urination， and dry stools， which were most pronounced in the Qi and Yin deficiency group. Grip strength decreased， peak activity time occurred earlier， total distance in the open-field test was reduced， and residence time was prolonged. Precordial temperature decreased （P<0.01）， while paw temperature increased （P<0.05）， and skin moisture and oil content were reduced （P<0.05， P<0.01）. In terms of disease-related indicators， compared with the blank group， fasting blood glucose was significantly increased （>16.7 mmol·L^-1） in the model and Qi and Yin deficiency groups， and blood lipid levels were significantly elevated （P<0.05）. Vascular-related factors ET-1， MCP-1， VCAM-1， and VEGF were significantly increased （P<0.05，P<0.01）， while IGF-1 was significantly decreased （P<0.01）. Pathological examination of the aortic valve showed valvular thickening and structural disorganization. Carotid artery examination revealed discontinuity of the intima， foam cell accumulation beneath the intima， disordered smooth muscle arrangement， and widened intercellular spaces. Compared with the model group， ET-1， MCP-1， and VEGF levels were significantly decreased in both the Qi and Yin deficiency group and the counter-syndrome group. The reductions in ET-1 and MCP-1 were more pronounced in the Qi and Yin deficiency group （P<0.01）， while the decrease in VCAM-1 was more significant in the counter-syndrome group （P<0.05）. Compared with the blank group， the Qi and Yin deficiency group showed significantly prolonged activated partial thromboplastin time （APTT）， thrombin time （TT）， and prothrombin time （PT） （P<0.01）. The erythrocyte deformability index （TK）， erythrocyte sedimentation rate， erythrocyte electrophoresis index， and whole blood low-shear viscosity all showed increasing trends. Vascular ultrasound revealed reduced arterial blood flow velocity， increased vascular resistance， and intimal thickening without plaque formation. The aortic intima showed no obvious overall thickening， with only occasional localized thickening and foam cell presence， and carotid artery injury was observed. ConclusionA rat model of DMA with Qi and Yin deficiency syndrome was successfully established using high-fat diet feeding combined with STZ injection and Yin-depleting herbal administration. Shenqi compound formula effectively alleviated Qi and Yin deficiency syndrome， regulated glucose and lipid metabolism， improved hemorheological and coagulation function， reduced vascular lesion severity， and demonstrated potential for early prevention and treatment of DMA.

ObjectiveThis paper aims to explore the action and molecular mechanism of modified Tongluo Tangtai Formula（MTLTT） on myelin damage in diabetic peripheral neuropathy （DPN） based on network pharmacology and in vitro experiments. MethodsThe chemical components of the MTLTT were retrieved from the Traditional Chinese Medicine Systems Pharmacology （TCMSP） database and literature， and the component targets were collected from the SwissTargetPrediction database. The targets of DPN were collected from the GeneCards， OMIM， Disgenet， and GEO databases. Gene ontology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） enrichment analyses were performed using the Metascape database， and a network diagram was constructed using Cytoscape software. The binding actions of core components with glycogen synthase kinase 3 beta （GSK-3β） and β-catenin were analyzed by Autodock Vina. An in vitro DPN model was established by high glucose-induced Schwann cells and dorsal root ganglion cells （SCs/DRGs）. The ultrastructural morphological changes of SCs and DRGs were observed by scanning electron microscope（SEM）， and the expressions of myelin-associated glycoprotein （MAG） and myelin basic protein （MBP） were detected by immunofluorescence staining. The mRNA and protein expression levels of MAG， MBP， myelin protein 0 （P0）， peripheral myelin protein 22 （PMP22）， and Wnt/β-catenin signaling pathway-related protein β-catenin， GSK-3β， Wnt family member 3α （Wnt3α）， and Wnt inhibitory factor-1 （Wif-1） were detected by real-time polymerase chain reaction （Real-time PCR） and Western blot. ResultsNetwork pharmacology analysis revealed that MTLTT components may treat DPN via the Wnt signaling pathway， involving key proteins such as GSK-3β， β-catenin and Wif-1. The molecular docking results indicate that atropine， apigenin， baicalein， isoflavanone， and albiflorin have good binding activity with GSK-3β， and that all 13 core components have stable binding activity with β-catenin. Cell experiments showed that compared with the blank group， SCs and DRGs in the model group exhibited severe morphological and structural abnormalities such as disintegration， shrinkage and axonal rupture， while these abnormal changes were improved after MTLTT intervention. Immunofluorescence results indicated that the fluorescence intensity of MAG and MBP was markedly decreased in the model group relative to the blank group（P<0.01）， while MTLTT treatment obviously upregulated the expression of MAG and MBP compared with the model group （P<0.01）. Real-time PCR and Western blot assays revealed that the expression levels of myelin-related molecules MAG， MBP， P0 and PMP22 were significantly reduced in the model group （P<0.05，P<0.01）， and MTLTT remarkably increased their expression levels （P<0.05）. In the Wnt/β-catenin signaling pathway， the mRNA levels of GSK-3β， Wif-1 and Wnt3α were elevated and β-catenin mRNA expression was declined in the model group （P<0.01）. Meanwhile， the protein expressions of GSK-3β and Wif-1 were upregulated， whereas those of Wnt3α and β-catenin were downregulated （P<0.01）. Compared with the model group， MTLTT at different doses reduced the mRNA and protein levels of GSK-3β and Wif-1 to varying degrees （P<0.05）， and distinctly enhanced the protein expression of Wnt3α and β-catenin（P<0.01）. ConclusionMTLTT can alleviate high glucose-induced myelin damage. Its protective mechanism may promote myelin repair by upregulating the expression of MAG， MBP， P0 and PMP22， and the therapeutic effect is possibly associated with the activation of Wnt/β-catenin signaling pathway.

Based on advancements in modern medical research regarding the intricate connection between the endocrine and exocrine functions of the pancreas， as well as the relationship between pancreatic functions and traditional Chinese medicine （TCM） spleen system， this paper discussed the categorization of the pancreas. It is proposed that the pancreas is neither a true zang organ nor a fu organ， but possessed the attributes of an extraordinary fu-organ and can be classified under the spleen. The spleen governs transportation and transformation， ascent of the clear and dispersion of essence， which encompasses the endocrine and exocrine functions， and pancreatic enzymes and glucose-regulating hormones form the material basis for the spleen's function of dispersing essence. Diseases of the pancreas exhibit characteristics of both zang-organ deficiency and fu-organ excess， so treatment should simultaneously supplement zang-organ disease and regulate fu-organ disease when pancreas showing endocrine and exocrine co-morbidities， with focus on restoring the pancreas （spleen）'s dispersing essence function. Therapeutic strategies include supplementing spleen qi， nourishing spleen yin to strengthen spleen earth， unblocking spleen collaterals， raising spleen yang， and removing spleen turbidity to support the spleen's dispersing essence function， so as to replenish the essential qi of zang-fu organs， ensure their distribution throughout the body， and improve the endocrine and exocrine functions of the pancreas.

A systematic review of the traditional Chinese medicine （TCM） literatures published over the past decade on blood glucose fluctuations in diabetes mellitus was conducted to summarize related TCM research progress of theories and prescriptions， so as to provide references for future TCM theoretical exploration， basic research， and clinical prevention and treatment. Blood glucose fluctuation is an independent risk factor for chronic complications of diabetes mellitus， with significant progress made in TCM theories and prescription studies targeting this condition. The TCM theories include "spleen-pancreas homology"， "liver controlling dispersion"， "small intestine transforming qi and separating purity from turbidity"， "Yi Qi Zhou Liu theory"， "Xuan Fu Qi Ye theory"， "Yin-fire theory" and so on， all of which emphasize "Qi". Prescription studies primarily utilize clinical trials， which evaluate plentiful indexes of blood glucose fluctuation such as the mean amplitude of glycemic excursion. Classical and self-formulated prescriptions are widely used， with various dosage forms such as decoctions， granules and capsules. "Qi-Yin deficiency" is the main syndrome of blood glucose fluctuation. Basic research focuses on mechanisms that improve blood glucose fluctuation and reduce chronic complications， such as the renin-angiotensin system regulating islet β cell's function， and the transforming growth factor-β₁ inhibiting organ fibrosis. However， there are still some deficiencies in the evidential support and syndrome study of TCM theories， in the high-level evidence-based evaluation， efficacy comparison among multiple dosage forms， and the integration of TCM theories with prescription's clinical research， in the quantities， multi-level verifications， blood glucose fluctuation model establishment and intervention criteria as well as prescription-syndrome correspondence of prescription's basic research， and in the collaboration between clinical and basic research. Despite these challenges， TCM offers a promising approach to improving blood glucose fluctuation and reducing chronic complications in diabetes mellitus， with its rich theories， diverse methods， and proven efficacy.

Diabetic lower extremity arterial disease(DLEAD)is characterized by a low rate of diagnosis,low awareness,low treatment rate,high disability rate,and high mortality.Due to a lack of comprehensive prevention and treatment strategies or an integrated technological system,DLEAD has become a bottleneck in the prevention and control of diabetes mellitus at present.Traditional Chinese medicine(TCM)treatment of DLEAD offers the advantages of syndrome differentiation,evidence-based treatment,and holistic regulation.However,it lacks a comprehensive understanding of the through-course pathogenesis and unified standardized syndrome criteria.TCM treatment of DLEAD exerts multi-target and multi-pathway network effects,but the advantageous links are still not fully understood.TCM treatments can delay the onset and development of DLEAD,but the efficacy evaluation system remains incomplete.Furthermore,there is a lack of high-quality evidence-based medical evidence and clinical consensus and guidelines.Therefore,based on the idea of zhi wei bing,or treating the disease before it develops,in Chinese medicine,and focusing on the prevention and control of DLEAD,we have constructed a synergistic technical system that integrates traditional Chinese and Western medicine for the prevention and control of DLEAD.This system integrates prevention,diagnosis,treatment,mechanisms,and applications,so as to enhance the clinical effects of DLEAD prevention and control,and to create a new paradigm for collaborative traditional Chinese medicine and western medicine in the field of chronic disease management.

Gut microbiota is the microbial community that is specifically planted in the human gut and interacts with the human body.It plays an important role in the human body by regulating the basal metabolism and immunity of the host to maintain the homeostasis of the human body.Once the intestinal flora is dysregulated,it can lead to multi-system diseases.Hashimoto's thyroiditis is an organ-specific autoimmune disease.The pathogenesis of Hashimoto's thyroiditis is complex and its incidence is increasing year by year,which is gradually becoming a serious public health disease affecting the world.In recent years,the relationship between gut microbiota and bridge onychitis has received extensive attention.A large number of studies have shown that the richness and diversity of intestinal flora in Hashimoto's thyroiditis patients are changed compared with healthy people.Studies have shown that traditional Chinese medicine therapy can play a role in treating this disease by regulating intestinal flora.This article systematically summarizes the relationship between the two and the effect of traditional Chinese medicine on the treatment of bridge onychitis by regulating intestinal flora,so as to provide some reference for research in this field.

Gut microbiota is the microbial community that is specifically planted in the human gut and interacts with the human body.It plays an important role in the human body by regulating the basal metabolism and immunity of the host to maintain the homeostasis of the human body.Once the intestinal flora is dysregulated,it can lead to multi-system diseases.Hashimoto's thyroiditis is an organ-specific autoimmune disease.The pathogenesis of Hashimoto's thyroiditis is complex and its incidence is increasing year by year,which is gradually becoming a serious public health disease affecting the world.In recent years,the relationship between gut microbiota and bridge onychitis has received extensive attention.A large number of studies have shown that the richness and diversity of intestinal flora in Hashimoto's thyroiditis patients are changed compared with healthy people.Studies have shown that traditional Chinese medicine therapy can play a role in treating this disease by regulating intestinal flora.This article systematically summarizes the relationship between the two and the effect of traditional Chinese medicine on the treatment of bridge onychitis by regulating intestinal flora,so as to provide some reference for research in this field.

In western medicine， the small intestine anatomically belongs to the digestive system and is also an important immune organ of the body. The innate immune system of the small intestine consists of a tissue barrier， innate immune cells， and innate immune molecules. The dysfunction of any part can cause metabolic disorders and eventually lead to diabetes. In the pathogenesis of diabetes， traditional Chinese medicine （TCM） has the theory of ''spleen deficiency causing diabetes''， which points out that the impaired spleen function results in inadequate transformation， impaired essence spread， and turbidity by essence accumulation， which is the core pathological link of blood glucose metabolism disorder in diabetes. In terms of the relationship between the small intestine and the spleen， the theory of TCM holds that the small intestine is located in the abdomen and the abdomen is dominated by the spleen. The digestion， absorption， and endocrine functions of the small intestine are also similar to the functions of spleen in governing movement and transformation and spreading essence by virtue of spleen Qi. Therefore， the anatomical and physiological functions of the small intestine in western medicine are closely related to the spleen in TCM. At the same time， the spleen is closely related to the innate immune function of the small intestine in TCM. The spleen participates in the generation and distribution of defense Qi， and the process of defense Qi playing the external function is similar to the process of the activation of the innate immune response. The spleen is also an important organ involved in fluid metabolism， which can cooperate with the lung and kidney to timely remove turbid fluid from the body. It can also work with the stomach as the hub of Qi ascending and descending and regulate the physiological activities of "clear Yang" and "turbid Yin"， so as to ensure the homeostasis of the internal environment of the body， which is the basis for maintaining the normal function of the innate immunity of the small intestine. Therefore， taking "spleen deficiency causing diabetes" as a bridge， the theory of TCM and western medicine were combined to explain the relationship between small intestinal innate immunity imbalance and the pathogenesis of diabetes from the perspective of TCM， which is helpful to understand the pathogenesis of diabetes in a deeper level and also provide a new perspective and new way for the prevention and treatment of this disease with TCM.

Atherosclerosis （AS） is a chronic inflammatory pathological process in which lipid and/or fibrous substances are deposited in the intima of arteries， and it is one of the pathological bases of many cardiovascular and cerebrovascular diseases. Endoplasmic reticulum stress （ERS） is a protective mechanism of cell adaptation. Moderate ERS can reduce abnormal protein aggregation and increase the degradation of misfolded proteins to repair and stabilize the internal environment， while excessive ERS can cause unfolded protein reaction， activate inflammation， oxidative stress， apoptosis， autophagy， and other downstream pathways， and lead to cell damage， or even apoptosis. A large number of studies have shown that ERS mediates a variety of pathological processes related to AS， affects endothelial cells， smooth muscle cells， macrophages， endothelial progenitor cells， and other cell components closely related to its occurrence and development， influences the progress of AS by regulating cell function， and promotes the formation of AS plaque， the transformation of stable plaque to unstable plaque， and the rupture of unstable plaque. Regulation of ERS may be a key target for the prevention and treatment of AS， and it is a research hotspot at present. Traditional Chinese medicine （TCM） believes that the origin of AS is the imbalance of Yin and Yang， the disharmony of Zangfu organs， and the abnormal operation of Qi， blood， and body fluid， which leads to the accumulation of phlegm， blood stasis， and other pathological products in the pulse channels， making the blood flow blocked or misfunction and causing the disease， which belongs to the syndrome of deficiency in origin and excess in superficiality. As the pathogenesis of AS is complex， and the symptoms are diverse， TCM has significant advantages in treating AS because of its multiple targets， multiple pathways， stable efficacy， strong individualization， and high safety. This paper systematically elaborated on the role of ERS in the occurrence and development of AS and summarized the mechanism research on the regulation and control of ERS by Chinese herbal monomer， Chinese herbal extract， Chinese herbal compound， and proprietary medicine， so as to provide a theoretical basis for clinical research and drug development in the prevention and treatment of AS.