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2026Year32Volume5Issue
- Abstract：Objective:To investigate the role of spinal manipulative therapy (SMT) in preventing progression and reducing the need for surgery in moderate-to-severe adolescent idiopathic scoliosis (AIS).Methods:This randomized controlled clinical trial was conducted at the First Affiliated Hospital of Zhejiang Chinese Medical University between January 1, 2022, and December 31, 2023. Overall, 118 AIS patients were randomly divided into 2 groups by simple randomization: one receiving SMT combined with brace treatment (SMTB group, 59 participants, SMT was given twice weekly, brace was worn for 23 h per day) and the other receiving brace treatment alone (BA group, 59 participants, brace was worn for 23 h per day). The primary outcome measure was the success rate after 12-month treatment. The secondary outcomes related to scoliosis, including the Cobb angle, angle trunk rotation (ATR), and Scoliosis Research Society-22 (SRS-22) score were measured. All the above indicators were subjected to subgroup analysis based on the degree of scoliosis (moderate and severe). Adverse events were observed and recorded.Results:Modified intention-to-treat analyses included 112 participants (SMTB group and BA group each had 56 participants, 101 girls and 11 boys; 15.11±1.69 years). The success rate was significantly higher in the SMTB group [78.6% (44/56)] than in the BA group [51.8% (29/56), P<0.01]. Among the secondary outcomes, SMTB group was more effective than BA group in reducing the Cobb angle (difference, –3.93; 95% confidence interval [CI], –6.11 to –1.74, P<0.05); SMTB group showed a greater reduction in ATR compared to BA group (difference, –2.34; 95% CI, –3.46, –1.22, P<0.05) and demonstrated superior efficacy to BA in improving SRS-22 score (difference, 6.57; 95% CI, 4.55 to 8.59, P<0.05). Subgroup analysis showed that SMT had similar efficacy in the treatment of moderate and severe AIS. Safety analyses did not differ significantly between the two groups (P>0.05).Conclusion:SMT appears to be safe and beneficial for moderate-to-severe AIS. (Trial registration No. NCT06648005)Keywords：adolescent idiopathic scoliosis;brace;spinal manipulative therapy;quality of life;randomized controlled trial43|0|0Updated：2026-08-04
- Abstract：目的：验证铁死亡在复发性流产（RPL）发病机制中的作用，并探讨黄芩素通过抑制铁死亡减轻 RPL 的作用。方法：以 CBA/J（n=60）与 DBA/2（n=50）交配小鼠建立 RPL 模型组，CBA/J 与 BALB/c（n=10）交配小鼠作为对照组。在胚胎发育第 0.5天至第 12.5 天（E0.5–E12.5），对 RPL 模型小鼠（每组 n=10）分别给予黄芩素（10 和 40 mg/kg）、铁死亡抑制剂（ferrostatin-1，5 mg/kg）和铁螯合剂（去铁胺，1 mg/kg）。检测妊娠结局及铁死亡相关指标。通过丙二醛（MDA）评估脂质过氧化水平，通过谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）活性测定抗氧化系统状态。检测 Fe2浓度分析铁积累情况，并用 Western blotting 检测关键蛋白表达。体外实验中，在 erastin 暴露条件下，向 HTR-8/SVneo 细胞补充不同浓度的黄芩素（0.1、0.2 和 0.4 μmol/L）。此外，使用 RSL3 和 si-RNA 分别抑制 HTR-8/SVneo 细胞中谷胱甘肽过氧化物酶 4（GPx4）或核因子红细胞 2 相关因子 2（Nrf2）的表达。检测 HTR-8/SVneo 细胞的细胞活力、细胞毒性、铁死亡相关标志物以及 Nrf2 和 GPX4 蛋白表达，以确定黄芩素抗铁死亡的信号通路。结果：黄芩素显著减轻了 RPL 小鼠的流产率（P<0.01）和胎盘损伤。此外，黄芩素抑制了小鼠胎盘铁死亡，表现为 MDA、铁含量、酰基辅酶 A 合成酶长链家族表达降低，GSH 和 GPx 水平升高（P<0.01），以及抗铁死亡相关蛋白（GPx4、SLC7A11 和 Nrf2）表达增加（P<0.01 或P<0.05）。在体外，不同浓度的黄芩素可恢复铁死亡诱导剂 erastin 所致 HTR-8/SVneo 细胞的损伤和脂质过氧化，但抑制 GPx4 会减弱黄芩素的保护作用（P<0.01）。此外，沉默 Nrf2 显著降低了 GPx4 的表达（P<0.01），并消除了黄芩素在 HTR-8/SVneo 细胞中介导的抗铁死亡效应。Keywords：妊娠丢失;黄芩素;Nrf2/GPx4;铁死亡;滋养层细胞25|0|0Updated：2026-08-04
- Abstract：目的：探讨姜黄素（Cur）对子宫腺肌症（AM）的治疗作用及其机制。方法：新生ICR小鼠通过他莫昔芬（TAM）诱导子宫腺肌症模型。将24只新生雌性小鼠按随机数字表法随机分为对照组、模型组（TAM 1 mg/kg/天，第2-5天）、低剂量和高剂量姜黄素治疗组（TAM 1 mg/kg/天，第2-5天；姜黄素分别为50和200 mg/kg/天，第13-15周），每组6只。通过小鼠热板实验、子宫组织切片的苏木精-伊红（HE）染色、Masson 染色和 E-钙粘蛋白、N-钙粘蛋白、基质金属蛋白酶（MMP）9 和 MMP 11 的免疫组化染色来评估姜黄素的效果等。转化生长因子β1（TGF-β1）诱导 Ishikawa（IK）细胞发生表型改变，并在姜黄素处理后，通过实时荧光定量PCR和蛋白质印迹法检测E-钙粘蛋白、N-钙粘蛋白、MMP 9、MMP 11和p-Smad3/Smad3的mRNA和蛋白表达。结果：体内研究表明，姜黄素显著提高了小鼠痛阈（P<0.01）。模型小鼠的子宫纤维化和异位腺体侵入程度显著高于对照组，高剂量姜黄素治疗后这些改变显著降低（P<0.01）。高剂量姜黄素通过抑制子宫组织中TGF-β1的产生，逆转了E-钙粘蛋白的下降以及N-钙粘蛋白、MMP 9和MMP11水平的升高（P<0.01）。体外研究中，姜黄素增强E-钙粘蛋白的蛋白表达，降低N-钙粘蛋白、MMP 9 和MMP11的蛋白表达（P<0.01）。姜黄素有效抑制TGF-β1诱导的IK细胞Smad3的磷酸化（P<0.01）。结论：姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化，进而治疗子宫腺肌症，这为非激素类药物治疗子宫腺肌症提供了一种新方法。Keywords：姜黄素;子宫腺肌症;上皮-间质转化;转化生长因子-β130|0|0Updated：2026-08-04
- Abstract：Objective:To investigate the effects and underlying mechanism of action of dihydroartemisinin (DHA) on ferroptosis in ovarian cancer (OC).Methods:In vitro, SKOV3 and A2780 cells were treated with different concentrations of DHA. The proliferative capacity of DHA-treated OC cells was determined using cell counting kit-8 assay, scratch test and clone formation assay. In addition, OC cells were treated with the ferroptosis inhibitor (ferrostatin-1; Fer-1) in combination with DHA to observe the changes in cell viability. To confirm the oxidative stress-inducing effect of DHA, levels of Fe2+, glutathione (GSH) and reactive oxygen species (ROS) were detected using Fe2+, GSH and ROS kits, respectively. Western blotting and quantitative PCR analyses were performed to detect the expressions of signal transducer and activator of transcription 3 (STAT3), recombinant solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4) at the protein and gene expression levels to determine stimulatory effects on ferroptosis. In vivo, in accordance with the random number table approach, nude mice with successful tumor loading were divided into vehicle and DHA (150 mg/kg) groups, with 3 mice in each group. Throughout the 10-day treatment period, the body weights and tumor volumes of the mice were documented. The STAT3, SLC7A11, and GPX4 protein expression levels were determined using Western blotting and immunohistochemistry, respectively.Results:DHA significantly reduced the viability of OC cells, and treatment with Fer-1 significantly increased the survival rate of OC cells (P<0.05 or P<0.01). Subsequent to the administration of DHA, the migration rate and clone formation ability of OC cells decreased significantly (P<0.01). Compared with control cells, DHA-treated OC cells exhibited increased Fe2+ and ROS levels (P<0.05 or P<0.01), whereas the GSH level decreased with DHA treatment (P<0.05 or P<0.01). DHA-treated OC cells exhibited significantly lower levels of STAT3, SLC7A11 and GPX4 mRNA and protein than control cells (P<0.05 or P<0.01). In nude mice, treatment with DHA significantly reduced tumor volume (P<0.05). According to Western blotting and immunohistochemistry results, DHA treatment downregulated the expressions of STAT3, SLC7A11, and GPX4 (P<0.05 or P<0.01).Conclusion:Treatment with DHA can inhibit OC cell proliferation and induce ferroptosis in OC, and these effects may be predominantly mediated via STAT3/GPX4 signaling pathway.Keywords：dihydroartemisinin;ferroptosis;ovarian cancer;Chinese medicine;STAT3/GPX4 axis17|0|0Updated：2026-08-04
- Abstract：目的：探讨槲皮素（quercetin，QE）对生精功能的改善作用，并通过体内实验阐明其潜在分子机制。方法：将30只6–8周龄雄性C57BL/6小鼠采用随机数字法随机分为5组（每组n= 6）：对照组、雷公藤甲素（triptolide，TP）模型组（0.1 mg/kg·d），以及不同剂量槲皮素干预组（25、50和100 mg/kg·d）。除对照组外，其余各组均给予TP诱导生精功能损伤，槲皮素干预组在此基础上同期给予QE。干预持续35天，覆盖1个完整的生精周期，并于第38天处死小鼠。采用H&E染色、TUNEL染色及Western blot检测Bcl-2、Bax和cleaved caspase-9的表达，评价生精细胞的病理损伤及凋亡情况。通过免疫荧光和Western blot检测紧密连接蛋白，包括ZO-1和JAMA，评估血-睾屏障（blood-testis barrier，BTB）完整性。采用Western blot检测PI3K、AKT及p-AKT的表达，观察PI3K/AKT信号通路变化。并结合网络药理学和分子对接模拟预测QE的分子作用机制，并进一步进行实验验证。结果：QE处理可显著改善TP诱导的睾丸损伤，增加生精上皮厚度和生精小管直径，并减少生精细胞凋亡（P<0.05或P<0.01）。QE还可改善BTB关键蛋白ZO-1和JAMA的分布及表达水平（P<0.05或P<0.01）。网络药理学和分子对接研究提示，QE可能通过影响PI3K-AKT信号通路发挥作用；Western blot结果显示AKT磷酸化水平升高（P<0.05或P<0.01）。结论：QE可通过上调PI3K-AKT信号通路，减轻TP诱导的生精功能障碍，减少生精细胞凋亡，并维持BTB结构完整性。QE可能成为治疗TP诱导生精功能障碍的潜在治疗药物。Keywords：槲皮素;生精功能障碍;PI3K/AKT信号通路;血-睾屏障17|1|0Updated：2026-08-04
- Abstract：Objective:To investigate the effect of sennoside A (SA) on atherosclerosis (AS) in type 2 diabetes mellitus (T2DM) mice and its underlying mechanisms.Methods:Sixty-one 9-week-old AopE-/- mice were randomly divided into 6 groups using the random number table: control, model (fed a high-fat diet for 4 weeks, followed by intraperitoneal injection of streptozotocin), SA low-, medium-, high-doses (15, 30, and 45 mg/kg per day, respectively for 8 weeks), and positive control groups (100 mg/kg metformin per day, for 8 weeks, 10 or 11 per group). The body weight and blood glucose levels of the mice were monitored regularly. Serum lipid content was measured using biochemical kits, and fasting insulin levels were qualified using ELISA kits. Aortic tissue was examined using Oil Red O, HE, Masson, and Picrosirius red stainings to observe the pathological changes. The mRNA expressions of CD31, VE-cadherin, α-smooth muscle actin (α-SMA) and vimentin were detected by RT-qPCR. The relative protein expressions of organic solute carrier partner (OSCP1), matrix metalloproteinase 9 (MMP9), vascular endothelial growth factor A (VEGFA) and p-ERK1/2 proteins were analyzed using Western blot. In vitro, endothelial cell dysfunction was induced using high glucose combined with oxidized low-density lipoprotein (ox-LDL). These cell groups included the blank control, model, different concentrations of SA (1, 30, 100 μmol/L), metformin (Met), OSCP1 knockdown, SA combined with OSCP1 knockdown, and OSCP1 overexpressing combined with SA groups. Cell morphology was observed under a microscope. Cell proliferation was assessed utilizing cell count kit (CCK)-8 assay, migration was evaluated with scratch test, and invasion ability was determined using transwell assay. The methods for mRNA and protein detection were the same as in vivo.Results:Animal experiments demonstrated that SA and Met improved blood glucose, lipid levels, and insulin sensitivity in T2DM mice, delayed AS progression, and reduced plaque area (P<0.05 or P<0.01). Compared with the model group, SA and Met treatment increased the expressions of CD31 and VE-cadherin, decreased the mRNA expressions of α-SMA and vimentin, and reduced the relative protein levels of OSCP1, MMP9, VEGFA and p-ERK1/2 (P<0.05 or P<0.01). Cell experiments showed that SA and Met can inhibit the morphological changes, excessive proliferation, migration, and invasion of endothelial cells induced by high glucose and ox-LDL (P<0.05 or P<0.01). The trends of mRNA and protein expression were consistent with the results of the animal experiments. In the si-OSCP1 and si-OSCP1+SA groups, mRNA levels of CD31 and VE-cadherin were increased, while α-SMA and vimentin mRNA levels were reduced (P<0.05 or P<0.01). Additionally, the relative expression levels of these proteins were downregulated (P<0.05 or P<0.01), and cellular morphological changes and excessive proliferation were reversed (P<0.01). However, OSCP1 overexpression resulted in the opposite effects (P<0.05 or P<0.01).Conclusions:SA reduces plaque area and stabilizes plaque in T2DM mice. Its anti-AS effects may be mediated through the downregulation of OSCP1/ERK1/2 signaling pathway, which helps reverse endothelial-to-mesenchymal transition.Keywords：sennoside A;type 2 diabetes mellitus;atherosclerosis;endothelial dysfunctions;organic solute carrier partner 119|1|0Updated：2026-08-04
- Abstract：Objective:To explore the effects of icaritin on pancreatic cancer cell proliferation and the mechanisms underlying cell death.Methods:Transcriptomic and lipidomic analyses were performed on the pancreatic cancer cell lines pancreatic carcinoma 1 (PANC-1) and ascites of the pancreas carcinoma 1 (ASPC1) treated with icaritin (0, 25 μmol/L) to profile global gene expression and lipid metabolism alterations. Key cholesterol biosynthesis genes were validated via quantitative reverse transcription polymerase chain reaction and Western blot. Additionally, cell viability was assessed using luminescent assays, while cytoplasmic vacuolization (paraptosis marker) was observed microscopically. Total cholesterol levels were quantified enzymatically, and lipid species (e.g., phosphatidylcholine, triglycerides) were analyzed by principal component analysis and pathway enrichment.Results:Icaritin significantly altered lipid metabolism in pancreatic cancer cells by elevating membrane lipids such as phosphatidylcholine, ceramide, sphingomyelin, and phosphatidylethanolamines (P<0.05). Concurrently, it reduced the levels of energy-supplying lipids including triglycerides, diglycerides, and acylcarnitines (P<0.05). There was also a notable decrease in cholesteryl ester 24:1 levels, which is consistent with the suppression of cholesterol biosynthesis (P<0.05 or P<0.01). Icaritin inhibited the proliferation of PANC-1 and ASPC1 cells by downregulating key cholesterol biosynthesis genes, such as 3-hydroxy-3-methylglutaryl coenzyme A reductase and squalene epoxidase genes (P<0.01).Conclusions:Icaritin disrupts lipid metabolism and inhibits cholesterol biosynthesis in pancreatic cancer cells, leading to non-apoptotic cell death. This novel mechanism of action provides new therapeutic possibilities for the treatment of pancreatic cancer and highlights its potential as a targeted anticancer agent.Keywords：icaritin;cholesterol biosynthesis;lipid metabolism;cell death;pancreatic carcinoma;Chinese medicine18|1|0Updated：2026-08-04
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Herbal and Botanical Review
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