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Volume 32 ， Issue 5 ， 2026
- 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：Objective:To verify effect of baicalein on recurrent pregnancy loss (RPL) and explore its mechanism via inhibition of ferroptosis.Methods:In vivo, CBA/J (n=60) mated DBA/2 (n=50) mice were established as RPL group, while CBA/J mated BALB/c (n=10) mice were regarded as control group. Baicalein (10 and 40 mg/kg), ferroptosis inhibitor (ferrostatin-1, 5 mg/kg) and iron chelator (deferoxamine, 1 mg/kg) were administered in the RPL mice model (n=10 per group) from embryonic day 0.5–12.5 (E0.5–E12.5). Pregnancy outcomes and ferroptosis related markers were detected. Lipid peroxidation was assessed by malondialdehyde (MDA) and antioxidant system was determined by glutathione (GSH), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity. The Fe2+ concentration was tested to analyze iron accumulation and Western blotting was performed to detect key protein expressions. In vitro, different concentrations of baicalein (0.1, 0.2, and 0.4 μmol/L) were supplemented under the exposure of erastin in HTR-8/SVneo cells. Moreover, RSL3 and si-RNA were used to suppress the expression of glutathione peroxidase 4 (GPx4) or nuclear factor erythroid 2-related factor 2 (Nrf2), respectively, in HTR-8/SVneo cells. Cell viability, cytotoxicity, ferroptosis related markers, protein expressions of Nrf2 and GPX4 were detected in HTR-8/SVneo cells to determine the signaling pathway of baicalein against ferroptosis.Results:Baicalein significantly attenuated fetal loss (P<0.01) and placental damage in RPL mice. Besides, baicalein reduced placental ferroptosis which manifested decreased MDA, iron content, Acyl-CoA synthetase long-chain family protein expression and enhanced GSH and GPx levels (P<0.01) as well as increased protein expressions that were resistant to ferroptosis (GPx4, SLC7A11 and Nrf2, P<0.01 or P<0.05). In vitro, different concentrations of baicalein restored a ferroptosis inducer-erastin induced HTR-8/SVneo cells damage and lipid peroxidation, but GPx4 inhibition diminished the protective effect of baicalein (P<0.01). Additionally, Nrf2 silencing notably decreased GPx4 expression (P<0.01) and abolished baicalein-mediated anti-ferroptosis effect in HTR-8/SVneo cells.Conclusion:Baicalein has a protective effect on RPL via inhibiting ferroptosis through Nrf2/GPx4 signaling axis.Keywords：pregnancy loss;baicalein;Nrf2/GPx4;ferroptosis;trophoblasts25|0|0Updated：2026-08-04
- Abstract：Objective:To investigate the therapeutic effects and mechanisms of curcumin (Cur) in adenomyosis (AM).Methods:A mouse uterine AM model was established by exposing ICR neonatal mice to tamoxifen (TAM). Female neonatal mice (day 1, n=24) were numbered and randomly divided into control, model (TAM 1 mg/kg per day, day 2 to 5), low- and high-doses Cur groups (TAM 1 mg/kg per day, day 2 to 5; Cur 50 and 200 mg/kg per day, respectively, week 13 to 15), by a random number table, with 6 mice in each group. The effect of Cur was assessed by a hot-plate test on mice and uterine sections for hematoxylin and eosin (HE), Masson staining, and immunohistochemistry staining of E-cadherin, N-cadherin, matrix metalloproteinases (MMP) 9 and MMP 11. Ishikawa (IK) cell phenotypic transformation was induced by transforming growth factor beta 1 (TGF-β1), and the mRNA and protein expressions of E-cadherin, N-cadherin, MMP 9, MMP 11 and p-Smad3/Smad3 were detected by quantitative real-time PCR and Western blot after Cur treatment.Results:In vivo study results showed that Cur significantly improved pain tolerance (P<0.01). The degrees of lesion fibrosis and invasion of ectopic glands in model mice were significantly higher than those in control mice, and the degrees were significantly reduced after high-dose Cur treatment (P<0.01). High-dose Cur reversed the decrease of E-cadherin and the increase of the levels of N-cadherin, MMP 9 and MMP11 by inhibiting the production of TGF-β1 in the uterine tissue (P<0.01). In vitro study, Cur increased the protein expression of E-cadherin and reduced the protein expressions of N-cadherin, MMP 9 and MMP 11 (P<0.01). Cur effectively inhibited the phosphorylation of p-Smad3/Smad3 in IK cells induced by TGF-β1 (P<0.01).Conclusion:Cur effectively alleviates AM and inhibits fibroblast differentiation and epithelial-mesenchymal transition by TGF-β1/Smad3 pathway, which provides a new approach for treating AM by non-hormonal drugs.Keywords：curcumin;adenomyosis;epithelial-mesenchymal transition;transforming growth factor-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：Objective:To investigate the ameliorative effects of quercetin (QE) on spermatogenic function and elucidate the underlying molecular mechanisms in vivo.Methods:Thirty male C57BL/6 mice (6–8 weeks old) were randomly divided into 5 groups using a random number (n=6 per group): control, triptolide (TP) model (0.1 mg/kg per day), and different doses of quercetin (QE) treatment groups (25, 50, and 100 mg/kg per day, intragastrically). Except for controls, all mice received TP to induce spermatogenic impairment, with concurrent QE administration in treatment groups. The intervention lasted 35 days, covering 1 complete spermatogenic cycle, and mice were euthanized on day 38. Histopathological damage and apoptosis in spermatogenic cells were evaluated using hematoxylin and eosin (H&E) staining, TUNEL assay, and Western blot analysis for Bcl-2, Bax, and cleaved caspase-9. Blood-testis barrier (BTB) integrity was assessed by immunofluorescence and Western blot for tight junction proteins, including zonula occludens-1 (ZO-1) and junctional adhesion molecule A (JAMA). The PI3K/AKT signaling pathway was investigated through Western blot analysis of PI3K, AKT, and phosphorylated AKT (p-AKT). Network pharmacology and molecular docking simulations were performed to predict QE's molecular mechanisms, followed by experimental verification.Results:QE treatment significantly ameliorated TP-induced testicular damage, increased spermatogenic epithelial thickness and spermatogonial tubule diameter, and decreased apoptosis of spermatogenic cells (P<0.05 or P<0.01). QE also improved the distribution and expression of key BTB proteins, including ZO-1 and JAMA (P<0.05 or P<0.01). Network pharmacology and molecular docking studies suggested that QE influences the PI3K-AKT signaling pathway, which was confirmed by increased AKT phosphorylation levels observed in Western blot results (P<0.05 or P<0.01).Conclusions:QE can mitigate TP-induced spermatogenic dysfunction, reduce apoptosis of spermatogenic cells, and preserve BTB structural integrity by upregulating the PI3K-AKT signaling pathway. QE may be a potential therapeutic agent for treating TP-induced spermatogenic disorders.Keywords：quercetin;spermatogenic disorder;PI3K/AKT signaling pathway;blood-testis barrier17|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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