Diabetic kidney disease （DKD） is one of the common microvascular complications of diabetes mellitus （DM） and a primary cause of chronic kidney disease （CKD） and end-stage renal disease （ESRD）. Inflammation is currently a hot topic in exploring the pathogenesis of DKD. Macrophages， T cells， interleukins， tumor necrosis factor， NOD-like receptor protein 3 （NLRP3） inflammasome， Janus kinase/signal transducer and activator of transcription （JAK/STAT） signaling pathway， and nuclear factor-kappa B （NF-κB）-related signaling pathway all play a role in regulating the inflammation of DKD and accelerating its progression. Astragali Radix， a Chinese herbal medicine， is widely used in the treatment of DKD and possesses strong anti-inflammatory effects. Studies have revealed that active ingredients of Astragali Radix， including polysaccharides， astragaloside Ⅳ， total flavonoids， calycosin， and quercetin， can regulate multiple signaling pathways to ameliorate the microinflammatory state and alleviate kidney damage， thereby slowing down the progression of DKD. This article systematically reviews the factors influencing the inflammation in DKD and analyzes recent research findings and mechanisms concerning active ingredients of Astragali Radix in the management of DKD inflammation， aiming to offer novel insights and directions for the prevention， treatment， and research of DKD.

Eight compounds were isolated and purified from the ethyl acetate part of 70% acetone extract of Rehmannia glutinosa by various chromatographic techniques such as silica gel, MCI gel CHP-20, ODS, Toyopearl HW-40C, combined with TLC and semi-preparative HPLC. Their structures were elucidated by modern spectroscopy techniques (NMR, MS, UV, IR), and identified as neomartynoside A (1), osmanthuside B₆ (2), martynoside (3), isomartynoside (4), (E)-p-hydroxycinnamic acid (5), caffeic acid (6), ferulic acid (7), and methyl caffeate (8). Compound 1 is a new phenylethanol glycoside, which was identified as neomartynoside A. Compound 2 was isolated from Rehmannia glutinosa for the first time. In addition, compounds 2, 6 and 7 significantly increased relative glucose consumption, showing potential hypoglycemic activity.

Granulation tissue hyperplasia after tracheotomy is a common clinical complication. Endoscopic treatment can temporarily relieve airway obstruction， however， it is associated with a high recurrence rate and poor long-term prognosis. Based on the traditional Chinese medicine （TCM） Kenang （窠囊） theory and combined with modern pathological mechanisms， this paper explores its correlation with the pathogenesis of post-tracheotomy granulation tissue hyperplasia. Drawing from clinical experience in applying the Kenang theory for treatment， this paper proposes that the fundamental pathogenesis of this condition lies in qi deficiency and organ dysfunction， while phlegm and blood stasis interlocking serve as the symptomatic manifestations. The treatment focuses on resolving phlegm and promoting blood circulation， dispersing nodules and eliminating stagnation， regulating qi flow， and reinforcing the body's vital energy while expelling pathogenic factors. This approach aims to dissolve phlegm and blood stasis， dissipate the Kenang， and ultimately prevent and treat granulation tissue hyperplasia.

ObjectiveTo observe the clinical efficacy and safety of Bushen Ruyan Formulation （补肾乳岩方， BRF） in treating premenopausal breast cancer patients of disharmony of the chong （冲） and ren （任） meridian type under endocrine intensive therapy. MethodsA total of 88 premenopausal breast cancer patients who received endocrine intensive therapy and were diagnosed with disharmony of the chong and ren meridian by traditional Chinese medicine （TCM） were included and randomly divided into a control group and a treatment group， with 44 cases in each group. The control group received ovarian function suppression （OFS） combined with endocrine therapy， while the treatment group was given oral BRF additionally. Both groups were treated for three months. The clinical efficacy was evaluated by comparing the pre- and post-treatment results of the Functional Assessment of Cancer Therapy-Breast （FACT-B）， modified Kupperman score， T cell subsets （CD3⁺， CD4⁺， CD8⁺， CD4⁺/CD8⁺）， sex hormone levels， including estradiol （E₂）， luteinizing hormone （LH）， follicle-stimulating hormone （FSH）， progesterone （P）， testosterone （T）， and prolactin （PRL）， tumor markers， such as carcinoembryonic antigen （CEA）， carbohydrate antigen 125 （CA125）， and carbohydrate antigen 153 （CA153）， TCM syndrome score， and TCM syndrome efficacy. Blood routine tests， liver function and kidney function were monitored to assess safety. ResultsThe FACT-B scores of each domains and the total scores of the treatment group increased， while the social/family status score of the control group decreased. The treatment group had significantly higher scores in all domains and total score compared to the control group （P＜0.05 or P＜0.01）. The modified Kupperman score and TCM syndrome score of the treatment group decreased， and were lower than those of the control group （P＜0.01）. The levels of CD3⁺ and CD4⁺ in the treatment group increased， and were higher than those of the control group （P＜0.05）. Serum testosterone levels in the treatment group were lower than those in the control group （P＜0.05）. The total effective rate of TCM syndrome efficacy in the treatment group was 67.44%， significantly higher than the 23.26% in the control group （P＜0.05）. No significant abnormalities were observed in the blood routine tests or liver/kidney function indicators in either group before or after treatment. ConclusionBRF can effectively improve quality of life， alleviate symptoms， increase serum CD3⁺ and CD4⁺ levels， and enhance clinical efficacy in premenopausal breast cancer patients undergoing endocrine intensive endocrine therapy. It is also safe with no significant adverse effects.

[摘 要] 目的：探讨同源框蛋白C4（HOXC4）在胃癌组织和细胞中的表达及其对胃癌细胞增殖、迁移与侵袭的作用及其机制。方法：收集2020年5月至2021年4月期间在南阳市第一人民医院肿瘤科手术切除的16例进展期胃癌患者的癌及癌旁组织标本，以及人胃正常上皮细胞GES-1和胃癌细胞AGS、SGC-790和MGC-803，采用WB法检测胃癌组织和细胞中HOXC4的表达。通过RNA干扰技术对SGC-790及AGS细胞中HOXC4进行敲低或过表达，实验分为sh-HOXC4#1组、sh-HOXC4#2组、sh-Con组、sh-HOXC4 + pc-integrin β1组、pc-HOXC4组、pc-Con组、pc-HOXC4 + pc-integrin β1组。利用EdU、CCK-8、Transwell实验分别检测敲低或过表达HOXC4对各组细胞活力、增殖、侵袭、迁移和integrin β1表达的影响。用敲低HOXC4的胃癌AGS细胞构建荷瘤小鼠模型，观察敲低HOXC4对移植瘤体积及组织中Ki67和integrin β1蛋白表达的影响。结果：胃癌组织和细胞中HOXC4的表达均显著上调（均P < 0.01）。与sh-Con组相比，sh-HOXC4#1组和sh-HOXC4#2组SGC-790及AGS细胞中HOXC4、integrin β1蛋白表达水平，以及细胞的活力、增殖、迁移及侵袭能力均显著降低（均P < 0.01）。与sh-HOXC4组相比，sh-HOXC4 + pc-integrin β1组细胞活力、增殖、迁移及侵袭能力均显著增加（均P < 0.01）；与pc-Con组相比，pc-HOXC4组细胞活力、侵袭及迁移能力均显著增加（均P < 0.01）；与pc-HOXC4组相比，pc-HOXC4 + pc-integrin β1组细胞活力、迁移及侵袭能力均显著降低（均P < 0.01）。与sh-Con组相比，sh-HOXC4#1组和sh-HOXC4#2组小鼠移植瘤生长缓慢、体积变小，组织中Ki67和integrin β1表达均显著降低（均P < 0.01）。结论：HOXC4在胃癌组织与细胞中表达上调，其通过激活integrin β1信号促进胃癌细胞的增殖、迁移与侵袭。

Based on the viewpoint of "sweat pore-qi and liquid-kidney collaterals"， it is believed that children's nephrotic syndrome is caused by the core mechanism of sweat pore constraint and closure， qi and liquid imbalance， and kidney collaterals impairment， and it is proposed that the treatment principle is to nourish the sweat pore， regulate qi and fluid， and supplement the kidney and unblock the collaterals. In clinic， guided by sequential therapy and according to the different disease mechanism characteristics of the four stages， including early stage of the disease， hormone induction stage， hormone reduction stage， hormone maintenance stage， the staged dynamic identification and treatment was applied. For early stage of the disease with edema due to yang deficiency， modified Zhenwu Decoction （真武汤） was applied to warm yang and drain water； for hormone induction stage with yin deficiency resulting in effulgent fire， modified Zhibai Dihuang Pill （知柏地黄丸） plus Erzhi Pill （二至丸） was used to enrich yin and reduce fire； for hormone reduction stage with qi and yin deficiency， modified Shenqi Dihuang Decoction （参芪地黄汤） was used to boost qi and nourish yin； for hormone maintenance stage， modified Shenqi Pill （肾气丸） was used to supplement yin and yang. Meanwhile， the treatment also attaches importance to the combination of vine-based or worm medicinals to dredge collaterals， so as to providing ideas for clinical treatment.

OBJECTIVE To investigate the ameliorative effects and potential mechanism of total secondary ginsenosides （TSG） on hypertrophic changes of primary cardiomyocytes stimulated by angiotensin Ⅱ （Ang Ⅱ）. METHODS Primary cardiomyocytes were isolated from the hearts of neonatal SD rats and divided into the following groups： control group， AngⅡ group （2 µmol/L）， TSG group （7.5 µg/mL）， PFK-015 group [6-phosphofructo-2-kinase/fructose-2， 6-bisphosphatase 3 （PFKFB3） inhibitor， 10 nmol/L]， and TSG+PFK-015 group （TSG 7.5 µg/mL+PFK-015 10 nmol/L）. The surface area， protein synthesis， energy metabolism-related indicators [free fatty acid （FFA）， coenzyme A （CoA）， acetyl coenzyme A （acetyl-CoA）]， and the expressions of glycolysis-related factors [hypoxia-inducible factor 1α （HIF-1α）， glucose transporter protein 4 （GLUT-4）， lactate dehydrogenase A （LDHA）， pyruvate dehydrogenase kinase 1 （PDK1） and PFKFB3] in primary cardiomyocytes of each group were measured. RESULTS Compared with the control group， the surface area of primary cardiomyocytes and protein synthesis were significantly increased， the content of FFA， protein and mRNA expressions of HIF-1α， LDHA， PDK1 and PFKFB3 were significantly increased or up-regulated in the AngⅡ group， while the contents of CoA and acetyl-CoA， the protein and mRNA expressions of GLUT-4 were significantly decreased or down-regulated （P＜0.05）. Compared with the AngⅡ group， both TSG group and PFK-015 group showed significant improvements in these indexes， with the TSG+PFK-015 group generally demonstrating superior effects compared to either treatment alone （P＜0.05）. CONCLUSIONS TSG can reduce the surface area of AngⅡ-induced primary cardiomyocytes， decrease protein synthesis， and inhibit their hypertrophic changes. These effects may be related to improving energy metabolism and the inhibition of glycolysis activity.

Myocardial ischemia-reperfusion injury （MIRI） is a common cardiac pathological process， resulting from the combined effects of multiple mechanisms involving metabolic changes and mitochondrial dysfunction. Mitochondrial quality control （MQC）， as a key regulatory mechanism， may serve as an important target for the prevention and treatment of MIRI. In recent years， traditional Chinese medicine （TCM） has demonstrated unique advantages in the field of improving MIRI， with multiple targets， multiple pathways， and low toxic and side effects. It has gained widespread clinical recognition and application. Through systematically organizing and summarizing recent studies on the targeting of MQC by monomers， active fractions， herb pairs， compound formulas and related preparations of TCM to improve MIRI， this paper finds that monomers and active fractions of TCM （such as schisandrin B， isoliquiritigenin， calenduloside E， berberine， Lycium barbarum polysaccharides and so on） as well as TCM herb pairs， compound formulas， and related preparations （couplet medicinals of Fuzi-Ganjiang， Yixin formula， Shuangshen ningxin capsule， Baijin formula， Yiqi huoxue decoction and so on）， can alleviate MIRI by activating MQC to reduce oxidative stress-induced damage， promote mitochondrial biogenesis， maintain mitochondrial fission/fusion homeostasis， regulate mitochondrial autophagy， and restore mitochondrial calcium homeostasis.

Chaihu Guizhi Ganjiangtang （CGG）is a classic prescription in the Treatise on Cold Damage，which has the effects of clearing and relieving stagnation heat in Shaoyang，warming and dissolving water drink，and relieving the pivot mechanism. It is a classic prescription for treating spleen deficiency and liver depression and stopping internal stagnation caused by water drink. The formula is exquisite and well-matched and is often modified and used by ancient and modern medical practitioners to treat various miscellaneous diseases of internal and external medicine，with significant therapeutic effects. In recent years，with the rapid development of modern pharmacology，research on the micro mechanism of CGG has been continuously developed and deepened，providing new ideas for the treatment of diseases with CGG. Therefore，the authors systematically searched databases such as China National Knowledge Infrastructure，Wanfang Data Knowledge Service Platform，VIP Database， and PubMed for literature on the clinical application and pharmacological mechanism of CGG published by Chinese and foreign scholars in recent years. This article summarized the literature from two aspects：the modern clinical application and mechanism of action of CGG and elaborated on the diseases treated by CGG in modern literature，involving digestive system，respiratory system，nervous system，endocrine system，circulatory system，urinary system，gynecology，as well as its application in reducing the side effects of radiotherapy and chemotherapy， gynecology， dermatology， ophthalmology， and orthopedics. At the same time，the mechanism of CGG in treating diseases may be related to anti-inflammatory，anti-oxidative stress， regulation of immunity， anti-fibrosis， anti-tumor， improvement of gastrointestinal flora and motility， protection of liver tissue， reduction of blood lipids and blood sugar， and regulation of hormone levels.

Cognitive impairment （CI） is a clinical syndrome characterized by progressive decline in advanced cognitive functions such as memory， thinking， and judgment. Its etiology and pathogenesis are complex， and there is currently a lack of specific drug interventions. Metformin， as a first-line hypoglycemic drug for type 2 diabetes， not only lowers blood glucose levels but also improves CI. This article reviews and summarizes the pharmacological effects and mechanisms of metformin in improving Alzheimer’s disease， diabetes cognitive impairment， cognitive impairment after chemotherapy， in order to provide novel insights and approaches for the treatment of CI-related diseases. Studies have shown that the mechanism by which MET intervenes in CI mainly includes regulating β-amyloid protein and tau protein metabolism， reducing insulin resistance， inhibiting neuroinflammation， improving synaptic plasticity， improving mitochondrial dysfunction， regulating gut microbiota and lipid metabolism， etc. Future research needs to be conducted through interdisciplinary collaboration， fully integrating multiple omics data， and combining advanced technologies to further reveal their mechanisms of effect.