Issue Ebook
cover story
Latest Issue
2026Year32Volume1Issue
- Abstract：目的:评价通心络胶囊在真实世界中对ST段抬高型心肌梗死 (STEMI) 患者中、远期预后的疗效与安全性.方法:本研究采用多中心、前瞻性队列研究方法, 在中国122家拥有胸痛中心的临床医院开展. 参与者依据接受再灌注术前或术后第1天是否使用通心络被自然分为暴露组 (n=1,598) 和非暴露组 (n=1,600) . 两组均接受基于指南指导的经皮冠状动脉介入治疗 (PCI) 或溶栓治疗. 主要终点是12个月时主要不良心脑血管事件 (MACCEs) 发生率. 次要终点包括30天时STEMI严重并发症发生率; 30天与6月时MACCEs发生率; 6月与12月时复合终点事件发生率; 30天、6月与12月时全因死亡率.结果:共有3198例患者被纳入主要分析. 主要终点即12个月时的MACCEs发生率在暴露组中显著降低[40(2.5%)vs.106(6.6%)], 主要原因归结于心源性死亡与脑卒中的减少. 次要终点分析中, 较非暴露组, 暴露组在30天[MACCEs: 19(1.2%)vs.64(4.0%)]和6月[MACCEs: 33(2.1%)vs.90(5.6%)]时的风险明显降低; 暴露组在30天STEMI严重并发症方面降低了92%[16(1.0%)vs.210(13.1%)], 包括心源性休克、急性心力衰竭、机械并发症和恶性心律失常的减少; 暴露组在6个月时[36(2.3%)vs.104(6.5%)]和12个月时[43(2.7%)vs.127(7.9%)]的复合终点事件分别降低了65%和66%, 其中心力衰竭再入院显著减少, 严重出血风险降低了89%. 令人惊喜的是, 暴露组在30天、6个月和1年时的全因死亡风险分别降低了71%、61%和59%.结论:联合通心络治疗在12个月的STEMI患+G2Keywords：通心络;中医;ST段抬高型心肌梗死;真实世界研究0|0|0Updated：2026-02-14
- Abstract：Objective:To evaluate the therapeutic effects of Kuanxiong Aerosol (KXA) on ischemic stroke with reperfusion and elucidate the underlying pharmacological mechanisms.Methods:In vivo pharmacological effects on ischemic stroke with reperfusion was evaluated using the transient middle cerebral artery occlusion (t-MCAO) mice model. To evaluate short-term outcome, 30 mice were randomly divided into vehicle group (n=15) and KXA group(n=15). Mice in KXA and vehicle groups received 69 mg KXA and vehicle for 1 day, respectively. To evaluate long-term outcome, 35 mice were randomly divided into sham group (n=5), vehicle group (n=15), and KXA group (n=15). Mice in KXA and vehicle groups received 69 mg KXA and vehicle for 7 days, respectively. Pathological changes in the brain were observed by 2,3,5-triphenyltetrazolium chloride or Nissl stainings, and behavioral assessments, including the Modified Neurologic Severity Score, Bederson score, rotarod test, and adhesive removal test were conducted. The penetration ability of KXA and KX (KXA without propellants) through the blood–brain barrier was assessed both in vitro using a transwell model and in vivo. Furthermore, in vitro effects of KX (5, 10, and 20 μL/L) on oxygen and glucose deprivation/re-oxygenation (OGD/R)-induced injury, transient receptor potential vanilloid type 1 (TRPV1) modulation, calcium influx, and mitochondrial function were explored through Western blot, CCK-8 assay, JC-1 staining, calcium imaging, adenosine triphosphate (ATP) and antioxidant measurements.Results:In in vivo experiments, KXA reduced brain infarct volume and neuron loss in t-MCAO mice. Behavioral assessments showed marked improvement in the neurological deficit of t-MCAO mice with KXA treatment (P<0.05 or P<0.01). Additionally, in vitro findings indicated that KX ameliorated OGD/R-induced injury through TRPV1 channel modulation. KX increased cell viability in OGD/R-treated SH-SY5Y cells and prevented OGD/R-induced calcium overload by downregulating TRPV1 expression and constraining calcium influx through TRPV1 (P<0.05 or P<0.01). Furthermore, KXA maintained the membrane potential and function of mitochondria in OGD/R-treated SH-SY5Y cells.Conclusions:KXA could attenuate ischemic stroke injury through TRPV1 channel modulation, indicating its potential as a promising therapeutic option for stroke in clinical practice.Keywords：stroke;transient receptor potential vanilloid type 1;Kuanxiong Aerosol;Chinese medicine0|0|0Updated：2026-02-14
- Abstract：考察复方丹参滴丸对多柔比星 (DOX) /曲妥珠单抗 (TRZ) 诱导的心脏毒性的改善作用, 并初步探讨其作用机制.方法:采用随机数字表法, 将18只SD大鼠分为正常组 (生理盐水) 、模型组 (DOX/TRZ) 和CDDP给药组 (DOX/TRZ+CDDP) , 每组6只. 除正常组外, 其余大鼠在前11天内隔天经尾静脉注射DOX, 共 6次. 一周后, 在11天内隔天腹腔注射TRZ, 同样共 6次. 在注射DOX/TRZ期间, CDDP组大鼠每日灌胃CDDP, 其余组灌胃等体积生理盐水, 持续给药36天. 末次给药后, 对所有大鼠进行超声心动图检查、检测血清生化指标, 并考察心脏组织病理变化; 同时收集大鼠粪便样本进行肠道菌群分析, 并采用非靶向代谢组学技术分析血浆代谢物.结果:超声心动图结果显示, DOX/TRZ可导致心脏功能障碍, 而CDDP干预显著缓解了该损伤 (P<0.05或P<0.01) . 生化检测结果进一步表明, DOX/TRZ引起左心室射血分数、缩短分数、心肌肌钙蛋白I、肌酸激酶、肌酸激酶-MB等心脏损伤相关指标升高, 而CDDP治疗显著降低了这些指标水平 (P<0.05或P<0.01) . 血浆代谢组学分析提示, 色氨酸代谢、三羧酸循环及苯丙氨酸代谢 通路被显著富集. 肠道菌群分析表明, CDDP干预提高了肠道微生物多样性, 并改变了特定菌群 (Clostridia_UCG-014和Lactobacillus) 的相对丰度.结论:CPPD能够改善DOX/TRZ诱导的心脏损伤, 其机制可能与调节Clostridia_UCG-014丰度, 影响色氨酸代谢途径, 抑制吲哚-3-羧酸水平增加犬尿氨酸水平, 从而发挥抗心脏毒性作用.Keywords：心脏毒性;多柔比星;曲妥珠单抗;复方丹参滴丸;多组学分析;中药0|0|0Updated：2026-02-14
- Abstract：Objective:To explore the potential of honeysuckle-derived exosome-like nanovesicles (HELNVs) for preventing cisplatin-induced acute kidney injury (AKI).Methods:The renoprotective efficacy of HELNVs against cisplatin-induced AKI was assessed in human kidney cell-2 (HK-2) cells exposed to 100 μmol/L cisplatin for 24 h, followed by HELNVs (50–200 μg/mL) for another 24 h; the optimal therapeutic concentration was determined as 100 μg/mL. At this concentration, oxygen species (ROS) levels were measured by flow cytometry. Male C57BL/6 mice received a single intraperitoneal injection of cisplatin (30 mg/kg) to establish an AKI model and were then computer-randomized into 3 groups (n=6 per group): control group, daily intraperitoneal administration of normal saline (0.9% NaCl); the cisplatin-injured group, same NaCl regimen; the HELNVs treatment group, daily intraperitoneal administration of HELNVs (30 mg/kg) for 5 consecutive days, with euthanasia on day 6. Renal accumulation of HELNVs was tracked by small-animal multispectral imaging (peak uptake at 8–10 h). Functional assessment included serum creatinine and blood urea nitrogen (BUN) quantified with an automated biochemical analyzer. Molecular analyses included enzyme-linked immunosorbent assay (ELISA) quantification of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor-α (TNF-α).Results:HELNVs significantly reduced ROS, inflammatory responses, and apoptosis in cisplatin-treated HK-2 cells (P<0.01). In cisplatin-induced AKI mice, HELNVs were efficiently absorbed by kidney cells, effectively prevented oxidative damage and mitochondrial dysfunction (P<0.01). Following treatment with 30 mg/kg HELNVs, serum creatinine and BUN levels were markedly reduced (P<0.01). ELISA results showed decreased levels of IL-1β, IL-6, and TNF-α, along with up-regulated IL-10 (P<0.01).Conclusion:HELNVs may serve as a promising therapeutic approach for ameliorating cisplatin-induced AKI, offering a potential novel treatment option for managing this condition in clinical settings.Keywords：honeysuckle-derived exosome-like nanovesicles;cisplatin-induced acute kidney injury;anti-inflammation;anti-apoptosis;mitochondrial function protection0|0|0Updated：2026-02-14
- Abstract：探讨地耳草 (Hypericum japonicum, HJ) 及其活性成分通过抗炎与抗凋亡作用减轻肝纤维化的治疗效果.方法:将24只小鼠随机分为4组: 对照组、模型组、地耳草-1mg/g组、地耳草-2mg/g组. 采用四氯化碳 (CCl4) 按5μL/g体重每周2次腹腔注射, 连续6周建立肝纤维化模型. 随后, 通过灌胃给予小鼠1mg/g或2mg/g地耳草水溶液, 评估其对模型小鼠肝病理损伤、肝功能指标及纤维化标志物的影响. 结合网络药理学、分子对接及真核转录组学分析, 明确地耳草关键活性成分 (如白桦脂酸、β-谷甾醇、槲皮素、山奈酚) 与核心靶点 (如B细胞淋巴瘤-2 (Bcl-2) 、肿瘤蛋白p53 (TP53) 、肿瘤坏死因子-α (TNF-α) ) 的相互作用及相关信号通路. 此外, 通过体外实验验证地耳草活性成分对CCl4损伤HepG2细胞活力、炎症细胞因子表达及凋亡通路的影响; 采用16S rRNA扩增子测序探究地耳草对肠道菌群结构与功能的调控作用.结果:体内实验显示, 地耳草干预可显著改善小鼠肝病理损伤, 降低肝功能指标水平, 并下调α-平滑肌肌动蛋白表达 (P<0.01) . 网络药理学与分子对接结果表明, 地耳草关键活性成分与Bcl-2、TP53、TNF-α等核心靶点具有较强的结合亲和力. 真核转录组学分析鉴定出地耳草调控的核心差异表达基因, 这些基因参与炎症反应调控及细胞外基质受体相互作用通路. 尽管地耳草干预未显著改变肠道菌群丰富度, 但可调控与肝纤维化密切相关的代谢及免疫功能. 体外实验中, 地耳草活性成分可显著提高CCl4损伤HepG2细胞的活力, 下调TNF-α和白细胞介素-6 mRNA表达, 并通过调控Bcl-2抑制线粒体凋亡通路 (P<0.01) . 其中, 白桦脂酸在降低天冬氨酸转氨酶和羟脯氨酸水平方面效果最显著并且通过抑制TNF-α、β-谷甾醇通过降低谷胱甘肽水平分别发挥抗纤维化作用.结论:地耳草及其活性成分具有抗肝纤维化相关的抗炎与抗凋亡作用, 有望成为肝纤维化靶向治疗的潜在候选药物.Keywords：地耳草;活性成分;肝纤维化;炎症;凋亡0|0|0Updated：2026-02-14
- Abstract：Objective:To investigate the anti-inflammatory effects and mechanisms of action of 4 steroidal alkaloids (ebeiedinone, imperialine, chuanbeinone, and peimisine) in Fritillaria.Methods:This study established a lipopolysaccharide (LPS)-induced inflammatory model using mouse leukemia cells of monocyte macrophage (RAW 264.7) cells. The cell toxicity, nitric oxide (NO) release, expression levels of inflammatory factors, and expression levels of anti-inflammatory mechanism proteins and mRNA of ebeiedinone, imperialine, chuanbeinone, and peimisine on RAW 264.7 cells were detected by cell counting kit-8 (CCK8) assay, Griess assay, enzyme-linked immunosorbent assay, Western blot, and real-time quantitative PCR, respectively. An acute lung injury (ALI) rat model was established. Hematoxylin and eosin staining was used to observe the morphological and pathological characteristics of lung tissue in each group of rats. The expression levels of inflammatory factors and anti-inflammatory mechanism proteins and mRNA in the ALI rat model induced by the 2 alkaloids (ebeiedinone, peimisine) were detected.Results:The 4 alkaloids reduced the release of NO, downregulated the expression of pro-inflammatory factors, regulated the expressions of the TIR domain-containing adapter protein inducing interferon-beta (TRIF), myeloid differentiation factor 88 (MyD88), nuclear factor kappa-B (NF-κB), and mitogen-activated protein kinases (MAPKs) signaling pathways in LPS-induced RAW 264.7 cells, exerting an anti-inflammatory effect (P<0.05 or P<0.01). Ebeiedinone and peomisine improved pulmonary edema and inflammation levels, regulated the expressions of MyD88, NF-κB, and MAPKs signaling pathways in the ALI rat model, exerting anti-inflammatory effects (P<0.05 or P<0.01).Conclusion:The 4 alkaloids of Fritillaria exert anti-inflammatory effects in vivo and in vitro through MyD88- and TRIF-dependent signaling pathways, thereby protecting rats from ALI.Keywords：Fritillaria;isosteroidal alkaloids;mouse leukemia cells of monocyte macrophage;inflammation;lipopolysaccharide0|0|0Updated：2026-02-14
- Abstract：Objective:To investigate cerebral vasorelaxation of total flavonoids of Chuzhou chrysanthemum(TFCC) in rats and its mechanism.Methods:Cerebral basilar arteries (CBA) of rats were isolated, and the vasodilation induced by TFCC (10–2,560 mg/L) following pretension with 100 nmol/L U46619 or 30 mmol/L KCl were measured using a pressure myograph system. Addition of H2S synthase cystathionine-γ-lyase (CSE) inhibitor dl-propargylglycine (PPG, 100 μmol/L), a large-conductance Ca2+-activated potassium (BKCa) channel blocker iberiotoxin (IBTX,100 nmol/L) and L-type Ca2+ channel blocker nifedipine (100 nmol/L) were added to determine the effect of pretreatment with the inhibitors on TFCC-induced vasorelaxation. KCl (30 mmol/L) was used as a contractile agent, TFCC (3.3–270 mg/L)-induced relaxation was detected by measuring the length of the long axis of rat cerebral vascular smooth muscle cells (VSMCs). Determination of the effect of pretreatment of VSMCs by IBTX or nifedipine on TFCC-induced cellular relaxation, and intracellular free Ca2+ concentration([Ca2+]i) was detected by fluorescent method. Endothelial cells (ECs) were co-cultured with VSMCs to observe the effect of endogenous H2S on TFCC-induced relaxation in VSMCs.Results:TFCC caused a concentration-dependent vasorelaxation in the rat CBA precontracted with KCl or U46619 (P<0.01). Endothelial removal markedly attenuated this vasodilation, but the remaining vasorelaxation was still significant (P<0.01). The TFCC-induced cerebral vasorelaxation was remarkably inhibited by PPG, IBTX and nifedipine (P<0.01). TFCC caused a significant relaxation of rat CBA VSMCs (P<0.01). Co-culture with wild-type cerebral ECs but not with cystathionine-γ-lyase-or 3-mercaptosulfotransferase-knockout ECs markedly enhanced TFCC-induced relaxation of VSMCs (P<0.05) and increased H2S content (P<0.01). TFCC decreased the [Ca2+]i in VSMCs (P<0.01), which was attenuated by PPG and IBTX.Conclusions:TFCC dilated rat CBA in both endothelium-dependent and -independent manner. Its endothelium-dependent dilation was probably involved in the blockade of L-type Ca2+ channels caused by endothelial H2S activating BKCa channels in VSMCs; its endothelium-independent relaxation was primarily from the direct blockade of the L-type Ca2+ channels in VSMCs.Keywords：total flavonoids of Chuzhou chrysanthemum;cerebrovasodilation;endothelial H2S;large-conductance calcium-activated potassium channel;L-type Ca2+ channel;Chinese medicine0|0|0Updated：2026-02-14
Original Article
- Abstract：Objective:To evaluate the clinical efficacy and safety of Xueshuantong Injection (Lyophilized)(XST) in reducing residual inflammatory risk (RIR) in patients with unstable angina (UA).Methods:This was a randomized, double-blind, parallel-controlled multicenter trial. Patients with UA were recruited from Xiyuan Hospital and Guang'anmen Hospital of the China Academy of Chinese Medical Sciences between January 2024 and March 2025. Eligible participants were randomly assigned to the treatment group (XST 500 mg, 30 cases) or the control group (XST 25 mg, 30 cases) in a 1:1 ratio. Both groups received intravenous XST for 10 consecutive days along with standard medical therapy. The primary outcome was change in C-reactive protein(CRP) level from baseline to post-treatment. Secondary outcomes included changes in interleukin-6 (IL-6), matrix metalloproteinase-9 (MMP-9), high-mobility group box 1 (HMGB1), vascular endothelial growth factor(VEGF), and von Willebrand factor (vWF), as well as the Canadian Cardiovascular Society (CCS) classification, and Chinese Medicine (CM) syndrome scores. Safety was evaluated by monitoring adverse event (AE) and performing laboratory tests of liver and kidney function before and after treatment.Results:A total of 59 patients completed the trial (30 in the treatment group and 29 in the control group). After treatment, the treatment group showed significantly greater reductions in CRP levels compared to the control group (P<0.01). In addition, the treatment group exhibited significantly improved IL-6, MMP-9, and HMGB1 levels, as well as CM symptom scores and CCS classification compared to the control group (all P<0.05). No serious adverse events were reported. Compared with the control group, the treatment group receiving XST showed greater improvements in RIR and clinical symptoms in UA patients with good safety and tolerability.Conclusion:XST shows potential to reduce RIR in patients with UA and may inform anti-inflammatory management. (Registration No. ITMCTR2025000552)Keywords：Xueshuantong Injection;unstable angina;residual inflammatory risk;randomized controlled trial;Panax notoginseng saponins;vascular inflammation0|0|0Updated：2026-02-14
Clinical Experience
Review
- 邮编：100091
- 联系电话：010-62886827, 62877592 传真：010-62874291
- 技术支持由北京北大方正电子有限公司提供 京ICP备05067934号-1
京公网安备11010802024621 - 本系统建议在Chrome、 IE9+ 以上版本浏览器阅读本站内容，360浏览器请切换至极速模式
- Cookies帮助我们提供服务并提供个性化体验。使用本网站，即表示您同意我们使用Cookies
0