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2026年第49卷第6期
Special Theme: TCM Prevention and Treatment of Kidney Disease
摘要：Based on the theory of treatment based on pathomechanism differentiation，this article proposes a diagnostic and therapeutic strategy for chronic kidney disease（CKD）from the perspective of common pathogenesis，in light of the pathological characteristics of its occurrence，progression，and outcome.It systematically demonstrates that renal collateral concretions and masses represent a common pathogenic mechanism throughout the evolution of different primary CKD entities.Its formation and progression follow a vicious cycle characterized by collateral damage leading to concretions and masses formation，and accumulated concretions and masses further damaging the collaterals，which continuously aggravates injury to the kidney collaterals during chronic disease，thereby driving persistent renal function decline and disease progression.On this basis，this article identifies dissolving concretions and dispersing masses as the core therapeutic principle for CKD，and further constructs a diagnostic and therapeutic approach integrating stage-based treatment with disease-specific treatment.Along the longitudinal course of disease progression，CKD is divided into early，middle，and late stages according to the dynamic pathomechanism evolution，which are treated respectively by unblocking collaterals and resolving concretions，activating blood and resolving concretions，and reinforcing healthy qi and resolving concretions.According to the pathological features of different primary kidney diseases，specific therapeutic method are proposed across the horizontal dimension of disease categories，including clearing heat and replenishing qi to dissolve concretions，activating blood and unblocking collaterals to dissolve concretions，and dispelling wind and eliminating dampness to dissolve concretions.This framework contributes to a holistic understanding of the complex evolution of CKD pathomechanisms and provides a systematic traditional Chinese medicine theoretical basis and practical clinical pathway for delaying disease progression and improving patient prognosis.关键词：chronic kidney disease;treatment on pathomechanism differentiation;common pathogenesis;renal collateral concretions and masses;dissolving concretions and dispersing masses72|42|0更新时间：2026-07-02Special Theme: TCM Prevention and Treatment of Kidney Disease
摘要：Persistent renal proteinuria is an independent risk factor leading to the deterioration of renal function and increased cardiovascular risk.Traditional Chinese medicine（TCM）holds certain advantages in preventing and treating renal proteinuria.Proceeding original TCM concepts such as " blood leaving the kidney channels becomes stasis" and " failure of the spleen to distribute essence result in turbidity，" our team advocates for understanding the TCM pathological nature of proteinuria from the perspective of " essence leaving the kidney channels，" positing that proteinuria is related to dampness turbidity.Pathogenic factors disturbing the kidney collaterals，dysfunction of qi transformation，and the formation of Zhengjia accumulations lead to essence failing to stay within the channels and the retention of dampness turbidity.This retention，in turn，further forms Zhengjia and brews toxins，accelerating the progression of chronic kidney disease." Treating turbidity to restore essence" is a key strategy in TCM syndrome differentiation and renal proteinuria treatment.Eight methods for syndrome differentiation and renal proteinuria treatment are proposed，including tonifying qi to recover essence，eliminating pathogens to protect essence，astringing to consolidate essence，dispelling dampness and draining turbidity，resolving Zhengjia and dispersing turbidity，dispelling wind and transforming turbidity，clearing heat and washing away turbidity，and promoting urination to remove turbidity.This article aims to expand the clinical thinking and diagnosis-treatment strategies for TCM in preventing and treating renal proteinuria.关键词：renal proteinuria;essence leaving the kidney channels;dampness turbidity;kidney collateral Zhengjia;treating turbidity to restore essence221|38|0更新时间：2026-07-02Special Theme: TCM Prevention and Treatment of Kidney Disease
摘要：IgA nephropathy（IgAN）is a common primary glomerular disease in China.The understanding of its pathogenesis remains limited，and existing theories are insufficient to fully elucidate the evolutionary process of the disease，from its insidious onset and progression to irreversible damage.Under the guidance of the " harmonizing sanjiao" theoretical system，our team innovatively proposes the" sanjiao-membrane source-kidney collaterals" pathogenesis hypothesis for IgAN.This theory posits that the pathogenic evolution of IgAN can be summarized as follows：initially，the dysfunction of sanjiao qi transformation serves as the root cause of the onset.Subsequently，damp-heat and toxic pathogens encumber the membrane source，accumulating to generate turbid toxins that attach and deposit，which acts as the pivot of the pathogenesis.Ultimately，the deeply latent turbid toxins back up against the kidney collaterals，leading to collateral spasm and the formation of micro-pelvic mass（microaccumulations），which is a consequence of the damage.This traditional Chinese medicine（TCM）pathogenic transmission process highly aligns with the " four-hit " hypothesis of IgAN in Western medicine.The dysfunction of sanjiao qi transformation is analogous to mucosal immune dysregulation and galactose-deficient IgA1 overproduction（the first hit）；the generation and deposition of damp-heat turbid toxins in the membrane source correspond to the pivotal transition involving the breakdown of immune tolerance，the formation of circulating immune complexes，and their deposition in the mesangial region（the second and third hits）；the mass formed by turbid toxins damaging the kidney collaterals microscopically resembles microthrombosis，chronic ischemia and hypoxia，and irreversible histological damage（the fourth hit）.Consequently，our team proposes a stratified intervention strategy，regulating the sanjiao to modulate qi transformation，freeing the membrane source to vent latent pathogens，and dredging the kidney collaterals to resolve pelvic masses.This theoretical and methodological framework integrates the theories of sanjiao qi transformation，latent pathogens in membrane source，and collateral disease theory.Combining these with the Western medical " four-hit " hypothesis provides a novel perspective for the precise prevention and treatment of IgAN using TCM.关键词：sanjiao;membrane source;kidney collaterals;IgA nephropathy60|60|0更新时间：2026-07-02Theoretical Studies
摘要：Standardization research on traditional Chinese medicine（TCM）syndrome must follow the specific principles of the discipline.It should adopt systems theories and thinking modes that are compatible with the complex holism of the TCM syndrome as well as the high-dimensional and high-order characteristics，to grasp the overall features of the syndrome and restore the cognitive pathways of treatment based on syndrome differentiation.The proposal of the basic features of syndrome，including" internal excess and external deficiency，dynamic time and space，and multi-dimension interfaces，"interprets the connotation of syndromology described by the field of informatics and lays an intellectual foundation for syndrome standardization.On this basis，this paper proposes the relationship between the basic features of the TCM syndrome and the standardization.From the perspective of interpretation of the characteristics of the TCM syndrome，the paper explores the guiding significance of the aforementioned three features for standardization practice and provides a preliminary exploration of practical approaches.The paper proposes that by applying a research approach that combines disease and syndrome to account for the feature of internal excess and external deficiency，the idea of syndrome differentiation of disease trend will thus reflect the features of dynamic time and space，while adopting dimension reduction and hierarchy elevation method to explore the analytical pathway of the multi-dimension interfaces.Based on the above rationale，considering the research process of the development of the diagnostic criteria for phlegm-stasis-toxin interjunction syndrome in acute ischemic stroke as an example，the corresponding practical pathway and key steps can be preliminarily summarized，with the aim of providing ideas and strategies for the standardization of research investigating TCM syndrome.关键词：syndrome;standardization;treatment based on syndrome differentiation;interpretation;features62|39|0更新时间：2026-07-02Experimental Studies
摘要：Objective To explore the biological significance of liver fibrosis（LF）with syndrome of liver yin deficiency in rats using metabolomics and transcriptomics，providing a scientific basis for a combined disease-syndrome model of LF.Methods According to body weight，30 male SD rats were divided into three groups（normal，model，and Zhibai Dihuang Pill groups），with 10 rats per group.The model and Zhibai Dihuang Pill groups received daily intragastric thyroxine suspension（80 mg/kg）and twice-weekly intraperitoneal injection of 50% CCl4 in olive oil solution（1.5 mL/kg）to induce LF with syndrome of liver yin deficiency.In the normal group，an equal volume of distilled water was administered by gavage，and an equal volume of olive oil solution was given by intraperitoneal injection.The Zhibai Dihuang Pill group also received daily Zhibai Dihuang Pill suspension（408 mg/kg）.Experimental procedures，including modeling and drug administration，were performed over two weeks.Liver weight and organ index were measured，and serum levels of alanine amino-transferase（ALT），aspartate transferase（AST），total bilirubin（TBIL），total bile acid（TBA），γ-glutamyltransferase（γ-GT），alkaline phosphatase（ALP），laminin（LN），hyaluronic acid（HA），transforming growth factor-β1（TGF-β1），and matrix metalloproteinase-2（MMP-2）were assessed.In liver tissue，tumor necrosis factor-α（TNFα），interleukin（IL）-1β，IL-6，IL-10，malondialdehyde（MDA），reduced glutathione（GSH），and the activities of catalase（CAT）and total superoxide dismutase（T-SOD）were evaluated.Hematoxylin and eosin（HE）staining was performed to examine liver damage，whereas Masson and Sirius red stainings were used to observe collagen fiber formation and distribution.Immunohistochemical staining was used to detect the positive expression of alpha-smooth muscle actin（α-SMA）in liver tissue.External indicators of syndrome of liver yin deficiency，including body weight，24 h food intake，24 h water intake，rectal temperature，tongue surface moisture content，and overall physical sign score（mental state，fur，stool，and urine scores），were assessed.Serum levels of cyclic adenosine monophosphate（cAMP），cyclic guanosine monophosphate（cGMP），triiodothyronine（T3），and thyroxine（T4）were measured，and the cAMP/cGMP ratio was calculated.The correlation analysis was performed between the tongue surface moisture content，rectal temperature and the related indicators of yin deficiency（serum cAMP，cGMP，T3，and T4）in the normal and model groups.Metabolomics and transcriptomics identified differential metabolites，expressed gene changes，and pathways in liver tissue between the normal and model groups，and the combined analysis of omics was performed.The adenosine monophosphate（AMP）content and the mRNA expression of aquaporin 7（Aqp7）in liver tissue were detected in the normal and model groups，and the correlation between them and the related indicators of yin deficiency was analyzed.Results The model group had significantly higher liver organ index and serum levels of ALT，AST，TBIL，TBA，γ-GT，ALP，LN，HA，TGF-β1，cAMP，T3，T4，and cAMP/cGMP ratio，and lower MMP-2 and cGMP levels compared to the normal group（P＜0.05）.In liver tissue，the contents of IL-10 and GSH and the activities of CAT and T-SOD decreased，whereas TNF-α，IL-1β，IL-6，and MDA levels increased（P＜0.05）.HE staining showed hepatocyte steatosis，ballooning degeneration，and fibrous tissue hyperplasia.Masson and Sirius red stainings indicated increased blue and red collagen fibers，with a significant rise in collagen and α-SMA area percentages in liver tissue（P＜0.05）.The 24 h water intake and rectal temperature rose，along with an increase in physical sign，mental state，fur condition，and urine scores；however，body weight，tongue surface moisture content，and stool score decreased（P＜0.05）.Compared with the model group，the Zhibai Dihuang Pill group reversed these indicators，except for body weight（P＜0.05）.In the normal and model groups，the tongue surface moisture content was very strongly negatively correlated with cAMP，T3，and T4，and very strongly positively correlated with cGMP（P＜0.05）；the rectal temperature was very strongly positively correlated with cAMP，T3，T4，and very strongly negatively correlated with cGMP（P＜0.05）.Liver tissue metabolomic analysis identified 247 significant metabolites primarily associated with the cGMPprotein kinase G and cAMP signaling pathways.Transcriptomic analysis identified 2，568 differentially expressed genes linked to transcriptional pathways，such as cytokine-cytokine receptor and extracellular matrix receptor interactions.Integrated omics analysis revealed key signaling pathways，including lipolysis regulation in adipocytes，ascorbate and aldarate metabolism，and purine metabolism.Experimental verification results showed that compared with the normal group，the AMP content and Aqp7 mRNA expression in the liver tissue of the model group were increased（P＜0.05）.The AMP content was very strongly positively correlated with cAMP，T3，and T4，and very strongly negatively correlated with cGMP（P＜0.05）.In contrast，Aqp7 was strongly positively correlated with cAMP，T3，and T4，and strongly negatively correlated with cGMP（P＜0.05）.Conclusion This study successfully developed an animal model of LF with syndrome of liver yin deficiency.Multi-omics verified that the pathological changes and syndrome manifestations in this model were consistent with clinical findings.Additionally，the study explains the syndrome and pathological mechanisms at metabolite and genetic levels，providing additional biological evidence for using this integrated disease-syndrome animal model.关键词：liver fibrosis;syndrome of liver yin deficiency;metabolomics;transcriptomics;model construction;rats52|36|0更新时间：2026-07-02Experimental Studies
摘要：Objective To observe the regulatory effect of Shoutai Pills on the senescence of endometrial stromal cells（ESCs）in mice with recurrent spontaneous abortion（RSA）and to explore how Shoutai Pills delay excessive senescence of ESCs and promote decidualization for fetal protection.Methods Eighty 6-8-week-old female CBA/J mice were randomly divided into the normal，model，Shoutai Pills（15.17g/kg），and dydrogesterone（3.00×10-3 g/kg）groups using a random number table method，with 20 mice per group.Once daily for 14 consecutive days；mice were caged at a female-to-male ratio of 2:1 for mating.Female CBA/J mice in the normal group were mated with male BALB/c mice，whereas those in the other three groups were mated with male DBA/2 mice to establish the RSA model.Pregnant mice continued to receive the corresponding treatments until gestational day 6，after which serum samples and decidual tissues were collected.HE staining was performed to observe the pathological changes of ESCs in decidual tissues；ELISA was conducted to determine the serum levels of decidualization markers，including insulin-like growth factor-binding protein 1（IGFBP1）and prolactin（PRL）；the senescenceassociated β-galactosidase（SA-β-gal）activity assay was used to evaluate the senescence status of ESCs.Immunohistochemistry，immunofluorescence staining，Western blotting，and quantitative reverse transcription PCR were employed to detect the protein and mRNA expression levels of IGFBP1，PRL，phosphorylated histone H2AX（γ-H2AX），phosphorylated P53 protein（p-P53），and cyclin-dependent kinase inhibitor 1A（P21）in decidual tissues.The remaining pregnant mice were treated until gestational day 10 for the statistical analysis of embryo loss rate.Results Compared with the normal group，the model group showed an increase in embryo loss rate（P＜0.05）；ESCs in decidual tissues were loosely and disorderly arranged，accompanied by reduced interstitial blood vessels and vacuolization in some cells；the protein and mRNA expression levels of IGFBP1 and PRL were downregulated（P＜0.05），with corresponding decreases in their serum concentrations（P＜0.05）；SA-β-gal activity was enhanced（P＜0.05）；and the protein and mRNA expression levels of γ-H2AX，p-P53 and P21 were upregulated（P＜0.05）.In contrast，compared with the model group，both the Shoutai Pills and dydrogesterone groups exhibited a reduction in embryo loss rate（P＜0.05）；ESCs in decidual tissues were tightly and neatly arranged，with abundant interstitial blood vessels and cytoplasm；IGFBP1 and PRL protein and mRNA expression levels were upregulated（P＜0.05），along with increased serum levels（P＜0.05）；SA-β-gal activity was attenuated（P＜0.05）；and the protein and mRNA expression levels of γ-H2AX，p-P53，and P21 were downregulated（P＜0.05）.Conclusion Shoutai Pills may exert a fetal protection effect by delaying the excessive senescence of ESCs and promoting the decidualization in mice with RSA.关键词：recurrent spontaneous abortion;Shoutai Pills;cellular senescence;decidualization;endometrial stromal cells;mice46|37|0更新时间：2026-07-02
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