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Volume 32 ， Issue 4 ， 2026
- Abstract：Objective:To evaluate the efficacy and safety of Tonifying Kidney-Yang Decoction (TKYD) in treating patients with vascular cognitive impairment (VCI) characterized by Shen (Kidney)-yang deficiency (SYD) syndrome.Methods:This multicenter, double-blind, randomized, and placebo-controlled clinical trial was conducted in 4 hospitals of China from September 2020 to December 2021. Eligible patients were enrolled and randomly assigned in a 1:1 ratio to receive either TKYD granules or placebo twice daily for 12 weeks. The primary outcomes were changes in scores of the Beijing Version of the Montreal Cognitive Assessment (MoCA-BJ) and Shen-Yang Deficiency Syndrome Scale (SYDSS) from baseline to week 12. The secondary outcomes included scores of the Mini-Mental State Examination (MMSE), Color Trails Test interference index, Stroop Color and Word Test-Stroop interference effect, Neuropsychiatric Inventory (NPI), Apathy Evaluation Scale-Clinician Version, and Activities of Daily Living scales. Safety was monitored throughout the trial.Results:A total of 120 patients completed the trial, including 63 and 57 in the TKYD and placebo groups, respectively. After 12 weeks of treatment, the TKYD group exhibited a significantly greater increase in MoCA-BJ (change: 1.40 vs. 0.11) and reduction in SYDSS scores (change: –12.17 vs. –7.46) than the placebo group (P<0.05 or P<0.01). Regarding specific domains of MoCA-BJ, TKYD exhibited significantly greater improvements in visuospatial/executive function, orientation and delayed recall (P<0.05 or P<0.01). In terms of change scores in SYDSS, TKYD also showed greater reductions in diarrhea before dawn, lumbago, and weakness of knees (P<0.05 or P<0.01). For the secondary outcomes, the TKYD group exhibited significantly higher MMSE scores and lower NPI scores compared with the placebo group (P<0.05 or P<0.01). No treatment-related adverse events were reported.Conclusion:TKYD is effective and safe for improving cognitive function and alleviating SYD symptoms in VCI patients with SYD syndrome. (Registration No. ChiCTR1900025713)Keywords：vascular cognitive impairment;Tonifying Kidney-Yang Decoction;Shen (Kidney)-yang deficiency;randomized controlled trial;cognitive function;Chinese medicine0|0|0Updated：2026-03-25
- Abstract：Objective:To investigate the action mechanism of Polygonatum sibiricum polysaccharides (PSP) in Alzheimer's disease (AD).Methods:Network pharmacology and molecular docking was used to identify the major active ingredients and potential targets of PSP in treating AD. Male Kunming mice were randomly divided into 6 groups by a simple randomization method: control, model, low-, medium-, and high-dose PSP, and donepezil groups (n=6 per group). An AD mice model was established by intraperitoneally injecting 120 mg/kg D-galactose and oral administration of 40 mg/kg AlCl3 for 70 d. PSP (100, 200, and 400 mg/kg) and donepezil (5 mg/kg) was administered orally for 35 d, respectively. Behavioral tests including the open field test, elevated plus maze, Morris water maze, and shuttle box test were performed to evaluate anxiety levels and learning and memory abilities. Western blot analysis was used to detect the phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signalling pathway activation. Leptin receptor (LepR) and neuronal nuclei (NeuN) co-localization was observed by immunofluorescence. Adeno-associated virus serotype 9 (AAV9)-mediated LepR knockdown (LepR-KD) was used to investigate the role of LepR in PSP-mediated cognitive improvement in AD mice and LepR and NeuN co-localization in the cerebral cortex. Immunohistochemistry was used to assess Tau protein deposition in the cortices of AD mice. Enzyme-linked immunosorbent assay quantified pro-inflammatory cytokines levels in the brain tissue.Results:Network pharmacology identified that PI3K-AKT was the key signalling pathway affected by PSP in AD mice. In vivo experiments showed that PSP significantly improved anxiety levels and cognitive learning abilities in AD mice, upregulated the expression ratios of p-PI3K/PI3K and p-AKT/AKT in brain tissue, enhanced the activity of LepR and NeuN, and reduced Tau protein accumulation and the expression levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (P<0.05 or P<0.01). LepR-KD further demonstrated that its deficiency attenuated PSP's neuroprotective effects on cognitive function and cortical neuronal survival.Conclusion:PSP modulates the PI3K-AKT signalling pathway in a LepR-dependent manner, thereby attenuating aberrant Tau protein deposition and inflammatory cytokine activity, which may cause delayed AD pathogenesis.Keywords：Polygonatum sibiricum polysaccharides;Alzheimer's disease;network pharmacology;PI3K-AKT;leptin receptor;Chinese medicine0|0|0Updated：2026-03-25
- Abstract：Objective:To explore the effects of Xinglou Chengqi Decoction (XCD) on severe traumatic brain injury (sTBI) and its relationship with gut microbiota.Methods:C57BL/6J mice were randomly allocated into sham, controlled cortical impact (CCI), and 3 doses of XCD (4.1, 8.2, and 16.4 g/kg) groups by using a random number table, n=7 per group. A CCI device was employed to establish the TBI model. XCD was administered intragastrically for 3 consecutive days. The effects of XCD on post-sTBI neurological deficits and histopathology were assessed. The contribution of gut microbiota to XCD-mediated improvement in sTBI was investigated using antibiotic-treated TBI mice. The gut microbiota-dependent mechanisms of XCD in sTBI were explored through 16S rDNA sequencing and serum metabolomics. The mechanisms underlying the absorbed ingredients of XCD in sTBI were examined using network pharmacology and metabolomics. Finally, mice were divided into sham, CCI, and flavin adenine dinucleotide (FAD)-treated groups, n=10 per group. FAD was administered to sTBI mice via daily tail vein injection (830 μg/kg) for 3 consecutive days to evaluate and verify its therapeutic effect.Results:XCD significantly mitigated neurological impairments, neuronal damage, apoptosis, and blood-brain barrier disruption in CCI model mice (P<0.05 or P<0.01). The medium dose (8.2 g/kg) exhibited the greatest effect. The gut microbiota partly contributed to these protective effects. 16S rDNA sequencing indicated that XCD promoted beneficial gut microbiota. Metabolomic analysis demonstrated that XCD regulated serum metabolic profiles, particularly FAD. Network pharmacology combined with metabolomics analysis revealed that the gut microbiota-independent components of XCD also targeted FAD in TBI. FAD exerted neuroprotective effects, improved energy metabolism, and promoted angiogenesis following TBI (P<0.05 or P<0.01).Conclusion:XCD exerts neuroprotective effects on sTBI through both gut microbiota-dependent and -independent mechanisms, which highlight the therapeutic role of FAD.Keywords：Xinglou Chengqi Decoction;traumatic brain injury;gut microbiota;metabolomic;flavin adenine dinucleotide;Chinese medicine0|0|0Updated：2026-03-25
- Abstract：Objective:To investigate the effect of Kai-Xin-San (KXS), alone and in combination with imipramine (IMI), to ameliorate treatment-resistant depression (TRD) by normalizing tryptophan (TRP) metabolism.Methods:Sixty Wistar rats were randomly divided into 6 groups using the lottery method (10 rats per group): control, adrenocorticotropic hormone (ACTH), IMI, KXS, KXS+IMI, and IMI+lithium (LIT). The control group received a vehicle solution, while the others were treated with ACTH (100 μg/d) for 14 days, and concurrently, KXS (365.4 mg/kg), IMI (10 mg/kg) and LIT (100 mg/kg) were administered to ACTH-treated rats for 15 days. The behavioral tests including forced swimming test (FST) and open-field test (OFT) were performed. The state of the hypothalamic-pituitary-adrenal (HPA) axis, the levels of key enzymes and critical products in TRP metabolism, the neuroinflammatory response and the expression of serotonin (5-HT) receptors, and the alterations in the glutamatergic signaling pathway were assessed. Furthermore, molecular docking was conducted to screen the major bioactive compounds in KXS.Results:Compared with the ACTH group, KXS and KXS+IMI effectively deceased the immobility time in FST (P<0.01), increased the total distance, number of standing, center time, and center entries in OFT (P<0.05 or P<0.01), and attenuated the serum levels of ACTH and corticosterone (P<0.05 or P<0.01). KXS and KXS+IMI mitigated the disturbances in TRP catabolism by increasing kynurenine amino transferases, tryptophan hydroxylase, 5-HT and kynurenic acid levels while attenuating tryptophan-2,3-dioxygenase (TDO), kynurenine-3-monooxygenase, kynurenine/TRP ratio, and quinolinic acid in hippocampus or liver (P<0.05 or P<0.01). Additionally, KXS and KXS+IMI not only reduced the levels of neuroinflammation and serotonin 2A receptor, also rectified abnormalities in the glutamatergic system by activating brain-derived neurotrophic factor-mammalian target of rapamycin pathway in hippocampus of ACTH-challenged rats (P<0.05 or P<0.01). Moreover, molecular docking indicated that pachymic acid, ginsenoside Rg1 and tenuifolin could bind to TDO.Conclusions:The therapeutic potential of KXS, especially combined with IMI, for TRD owed to its safeguarding effects on TRP metabolism. Pachymic acid, ginsenoside Rg1 and tenuifolin may be the primary contributors to these protective impacts of KXS.Keywords：Kai-Xin-San;treatment-resistant depression;therapeutic effect;tryptophan metabolic regulation;molecular docking;Chinese medicine0|0|0Updated：2026-03-25
- Abstract：Objective:To investigate the effect of Tiaobu Xinshen Recipe (TXR) on cognitive function of 5xFAD transgenic mice and explore the potential mechanisms.Methods:Six-month-old male wild-type (WT) mice and 5xFAD transgenic mice were randomly divided into vehicle (0.9% NaCl), TXR (granules, 4.18 g/kg) and donepezil (0.625 mg/kg) groups using a random number table, respectively, which were given intragastric administration once a day for 60 d. Spatial learning and memory performance was tested with modified Morris water maze (MMWM) test. Synaptic ultrastructure in the hippocampal CA1 region was observed by transmission electron microscopy. The levels of amyloid β (Aβ), the major amyloid precursor protein (APP)-cleaving enzymes and Aβ-degrading enzymes including β-secretase, α-secretase, neprilysin (NEP) and insulin-degrading enzyme (IDE), were detected by immunohistochemistry staining and Western blot, respectively.Results:In MMWM test, when compared with the 5xFAD-vehicle group, 5xFAD-TXR group demonstrated a significantly shorter escape latency to the platform and increased number of platform crossings and time spent in target quadrant (P<0.05 or P<0.01). The ultrastructure of synapse in the hippocampal CA1 region of mice in the 5xFAD-TXR group was significantly changed, including increased numbers of mitochondria and synaptic vesicles, intact synaptic membrane, and thickened postsynaptic density. The Aβ load was markedly decreased in the cerebral cortex and hippocampus CA1 subregion of TXR-treated 5xFAD mice (P<0.05). TXR treatment decreased APP levels and increased IDE expression in brains of 5xFAD mice (P<0.01). However, TXR treatment had no effect on α- and β-secretase, and NEP in 5xFAD mice (P>0.05).Conclusion:TXR improves cognitive dysfunction in 5xFAD mice by alleviating synaptic ultrastructure degradation and reducing Aβ.Keywords：Alzheimer's disease;amyloid β;cognitive deficit;synaptic ultrastructure;transgenic mice;Tiaobu Xinshen Recipe;Chinese medicine0|0|0Updated：2026-03-25
- Abstract：Objective:To explore the molecular mechanism by which protein tyrosine phosphatase 1B (PTP1B) enzyme regulates insulin resistance (IR) in diabetes mellitus, and the regulation of isoquercitrin (IS) on PTP1B in vitro and in vivo.Methods:In vitro, PTP1B overexpression plasmid was constructed and transiently transfected into human hepatocellular liver carcinoma (HepG2) cells. A co-inducer was prepared by mixing a 0.125 mmol/L palmitic acid solution with a 1.0×10-7 mol/L insulin solution to induce IR cell mode. Glucose oxidase assay, quantitative real-time-polymerase chain reaction (qRT-PCR), and Western blot were used to detect the effects of 40 μmol/L IS on glucose uptake and mRNA and protein expressions of related factors on the insulin receptor substrate (IRS)/phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signal pathway in the PTP1B overexpressed IR cell model, respectively. In vivo, PTP1B overexpression adeno-associated virus (Aav-PTP1B) was constructed and injected into the tail vein of mice (200 μL/piece). The metabolic indicators of mice were measured after 14-d intragastric administration of IS (40 mg/kg). The pancreas tissue was excised to observe the morphology via hematoxylin-eosin staining. Additionally, qRT-PCR and Western blot assays were performed on the liver tissue of mice to determine the expressions of related factors on the IRS/PI3K/AKT signal pathway of db/db and wild type mice after the intervention of IS on Aav-PTP1B.Results:In both in vivo and in vitro experiments, IS significantly improved IR, reduced levels of blood glucose, total cholesterol, triglycerides, and other metabolic indicators in mice, effectively controlled body weight, and restored pancreatic cell morphology (P<0.05 or P<0.01). At the genomic level, IS improved the expressions of related factors in the IRS/PI3K/AKT signaling pathway by regulating the expression of PTP1B (P<0.05 or P<0.01), thereby maintaining the homeostasis of the pathway.Conclusion:IS can improve IR by inhibiting the IRS/PI3K/AKT signaling pathway through PTP1B intervention.Keywords：insulin resistance;isoquercitrin;Chinese medicine;protein tyrosine phosphatase 1B;insulin receptor substrate/phosphatidylinositol-3-kinase/protein kinase B signal pathway0|0|0Updated：2026-03-25
Original Articles
Ethics Study
- Abstract：槲皮素及其衍生物是一种主要来源于天然水果和蔬菜的黄酮类化合物, 具有显著的抗氧化、抗炎和神经保护作用, 有助于预防和治疗各种认知障碍. 鉴于认知障碍的多因素病因, 本文综述了槲皮素及其衍生物对与阿尔茨海默病、代谢紊乱、帕金森病、血管疾病、应激、金属毒性和PM2.5暴露相关的认知功能下降的影响. 此外, 槲皮素与纳米材料的结合提高了其生物利用度. 然而, 槲皮素衍生物的种类有限, 其作用机制尚不明确, 以及剂型开发的限制, 强调了继续对槲皮素及其衍生物进行研究以预防和治疗多种认知功能障碍的必要性.Keywords：槲皮素;认知功能障碍;神经保护0|0|0Updated：2026-03-25
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Herbal and Botanical Reviews
- Abstract：慢性阻塞性肺疾病 (COPD) 是一种以不可逆性气流受限、进行性肺功能减退为特征的致残性呼吸系统疾病, 最终可引发心肺并发症及呼吸衰竭. 作为全球第三大死亡病因, COPD 在 40 岁以上人群中的患病率为 9%~10%, 且流行病学趋势呈逐年上升态势. 诱发 COPD 的主要危险因素包括吸烟、环境污染, 以及煤矿开采、建筑施工、纺织生产、粮食加工等职业暴露. 当前主流药物治疗手段 (包括支气管舒张剂, 如 β₂受体激动剂、抗胆碱能药物, 以及糖皮质激素) 尚无法阻断疾病进展. 支气管舒张剂存在明确不良反应: β₂受体激动剂可引发心动过速、肌肉震颤及代谢紊乱; 抗胆碱能药物则可能导致视物模糊、口干、尿潴留、认知障碍、直立性低血压与心律失常长期使用糖皮质激素会升高感染风险, 还可诱发高血糖、骨质疏松及神经精神系统疾病. 中医药在 COPD 防治中拥有悠久的临床应用历史, 其疗效也日益得到现代循证医学研究的验证. 近期临床研究表明, COPD 患者经补肺活血胶囊治疗 12 个月后, 6 分钟步行距离 (6MWD) 较基线平均增加 36.65 m, 疲劳、呼吸困难症状减轻, 肺功能 (第一秒用力呼气容积 FEV₁、用力肺活量 FVC) 改善, 咳嗽、咳痰症状消失率达 24.4%. 另一项多中心随机对照试验 (RCT) 证实, 金水六君汤合生脉汤联合噻托溴铵具有协同疗效. 治疗 12 个月后, 联合组在 FEV₁/FVC 改善、咳痰症状缓解方面均显著优于噻托溴铵单药组, 凸显了中西医结合方案在延缓肺功能下降中的优势. 此外, 中成药疗效对比与证据整合研究亦取得进展: 在常规治疗基础上联用中成药时, 固肾定喘丸在临床有效率相对风险上排名第一, 且 FVC 改善效果最优; 苏黄止咳胶囊在提升 FEV₁方面表现突出; 百令胶囊则在降低急性加重频次、改善 FEV₁/FVC 比值上更具优势. 从作用机制而言, 中医药干预可调控气道与肺部炎症、减轻气道重塑及高反应性、恢复氧化应激平衡、重建蛋白酶 - 抗蛋白酶系统平衡、纠正免疫功能紊乱. 本文就中医药调控 COPD 相关关键通路 (包括 p38 MAPK、PI3K/Akt、Wnt、NF-κB、NRF2 及 JAK/STAT 通路) 的最新研究成果进行综述, 并探讨拓展中医药治疗 COPD 的潜在新型研究策略.Keywords：慢性阻塞性肺疾病;中医药;信号通路;调控;研究进展0|0|0Updated：2026-03-25
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