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Volume 32 ， Issue 11 ， 2026
- Abstract：Objective: To evaluate the efficacy and safety of Zhangyanming Tablets (ZYMT) combined with 0.1% sodium hyaluronate eye drops for dry eye disease (DED). Methods: A stratified, randomized, doubleblind, placebo-controlled multicenter trial was conducted from June 2022 to August 2024, enrolling 144 patients with DED from 3 centers. Participants were randomized 1:1 to either the ZYMT group (ZYMT + 0.1% sodium hyaluronate, n=72) or the control group (placebo + 0.1% sodium hyaluronate, n=72). Participants received the study tablets (2 tablets orally, 3 times daily) concurrently with the eye drops (1 drop, 5 times daily) for 8 weeks. The primary outcome was the mean change from baseline in the ocular surface disease index (OSDI) score. The secondary outcomes included the efficacy rate, the mean change from baseline in the tear film breakup time (TFBUT), Schirmer's test, corneal fluorescein staining (CFS) and Chinese medicine (CM) syndrome score. Safety was assessed by monitoring adverse events, vital signs, and laboratory parameters (hematology, urinalysis, liver and kidney functions, and electrocardiogram). Results: A total of 119 patients completed this study, among which 58 were in the ZYMT group and 61 were in the control group. After 8 weeks of treatment, the mean change from baseline in the OSDI score in the ZYMT group was significantly greater than those in the control group in week 8 [absolute difference -5.66, 95% confidence interval (CI), -9.56 to -1.76]. The efficacy rate was 62.1% (36/58) in the ZYMT group versus 42.6% (26/61) in the control group (relative risk: 1.46, 95% CI, 1.02 to 2.08). The mean changes from baseline in TFBUT and CM symptom score were significantly greater in the ZYMT group than those in the control group at week 8 (P＜0.05). No significant differences were observed between the two groups in Schirmer's test, CFS, or safety data (all P＞0.05). Conclusion: ZYMT combined with 0.1% sodium hyaluronate eye drops can significantly alleviate the ocular symptoms, improve tear film, and demonstrate a good safety. (Registration No. ChiCTR2200061479)Keywords：dry eye disease;Zhangyanming Tablets;ocular surface disease index;tear film breakup time;Chinese medicine;double-blind trial56|5|0Updated：2026-11-13
- Abstract：Objective: Shexiang Baoxin Pill (MUSKARDIA) reduces major adverse cardiovascular events (MACE) and improves angina, this study aims to evaluate its differential efficacy across varying hemoglobin (Hb) levels. Methods: This was a subgroup analysis of a multicenter, randomized, double-blind, placebo-controlled phase Ⅳ trial. Patients with coronary artery disease (CAD) were stratified into two groups based on baseline Hb levels: Group A (Hb 140 g/L, n=1, 286) and Group B (Hb＞140 g/L, n=1, 208). The primary endpoint was MACE; secondary endpoints included non-fatal myocardial infarction (MI), non-fatal stroke, and all-cause mortality. Hazard ratios (HR) with 95% confidence intervals (CI) were estimated using Cox proportional hazards models. Results: In Group A, MUSKARDIA significantly reduced MACE risk (HR=0.45, 95% CI: 0.21-0.96, P=0.038), with a 68% reduction in non-fatal MI risk (P=0.036). Non-fatal stroke and all-cause mortality showed no significant differences. Adverse events were lower in the MUSKARDIA group (15.9% vs. 17.6%). In Group B, no significant MACE benefit was observed (P=0.354), with a trend toward increased non-fatal MI risk (HR=1.88). Non-fatal stroke and all-cause mortality were similar between groups. Adverse events were slightly higher (21.2% vs. 18.3%). Conclusions: MUSKARDIA demonstrated significant cardiovascular protective effects in CAD patients with Hb 140 g/L, particularly reducing non-fatal MI risk, while showing limited efficacy in patients with Hb＞140 g/L. This highlights its cardiovascular protective role in high-risk populations characterized by greater ischemic risk and inadequate myocardial oxygen supply.Keywords：chronic stable coronary artery disease;hemoglobin levels;MUSKARDIA31|0|0Updated：2026-11-13
- Abstract：Objective: To investigate the pharmacodynamic and pharmacokinetic interactions between Shenqi Oral Liquid (SQ) and atorvastatin (ATV) in hyperlipidemic rats, explore the impact of SQ on ATV-related transporters and metabolic enzymes, the potential implications for the safety and rationality of their combined administration based on pharmacodynamic, pharmacokinetic, transporter, and metabolic enzyme data. Methods: Hyperlipidemic rats were induced using a high-fat diet and randomized according to serum total cholesterol levels using a randomized block design into model, ATV (10 mg/kg), SQ (0.68, 1.68, 3.38 g/kg), and combination groups, and treated for 4 weeks. Serum lipid profiles, liver histopathological changes, pharmacokinetic parameters of ATV, mRNA expression levels of transporters (including Bcrp, Mrp2, etc.) and metabolic enzymes (CYP2C11, CYP3A2), enzyme activities, as well as the effects of SQ's active ingredients were assessed using quantitative PCR, cocktail probe assays, and primary hepatocyte studies. Results: The combination therapy significantly reduced serum lipid levels and improved liver histology, as evidenced by a more organized cellular structure and reduced accumulation of lipid droplets. SQ significantly increased systemic exposure of ATV metabolites, elevating the maximum plasma concentration (Cmax) and area under the curve from time 0 to time t (AUC0-t) of o-ATV by 97.02% and 119.01%, and of p-ATV by 73.22% and 63.39%, respectively (all P＜0.05). SQ downregulated the expressions of Bcrp and Mrp2 in the jejunum and Oatp2b1, Bcrp, and Mrp2 in the ileum, while upregulating Oatp1b2 and CYP3A2 in the liver (all P＜0.05). Additionally, it enhanced the enzymatic activities of CYP2C11 and CYP3A2, as shown by significantly reduced AUC0-∞ of omeprazole (P＜0.01) and AUC0-t of midazolam (P＜0.05). Notably, tangshenoside Ⅰ, lobetyolin, and ononin were found to promote CYP3A2 mRNA expression (P＜0.05). Conclusions: SQ synergizes with ATV in lipid regulation and hepatoprotection through modulation of drug transporters and metabolic enzymes. These findings suggest that dose adjustment of ATV may be necessary during combination therapy, thereby providing a scientific basis for the rational co-administration of these agents.Keywords：herb-drug interaction;pharmacodynamics;pharmacokinetics;metabolic enzymes;transporters;Shenqi Oral Liquid39|0|0Updated：2026-11-13
- Abstract：Objective: To investigate berberine (BBR) promotes mitochondrial biogenesis via the silent mating type information regulation 2 homolog 1/peroxisome proliferator-activated receptor gamma coactivator 1 alpha (SIRT1/PGC-1α) signaling pathway to exert its anti-atherosclerosis effects. Methods: A total of 42 8-week-old AopE-/- mice were fed a high-fat diet for 12 weeks, and then randomly divided into 7 groups via a simple randomization method: the model group, the low-, medium- and high-dose BBR groups [BBRL 50 mg/(kg·d), BBRM 100 mg/(kg·d) and BBRH 150 mg/(kg·d), respectively], positive control group [atorvastatin, 3 mg/(kg·d)], BBR combined with nuclear respiratory factor 1 (Nrf1) inhibitor group (BBRH+EX527, 150 mg/kg BBR+10 mg/kg EX527), and Nrf1 inhibitor group [EX527, 10 mg/(kg·d)]. Six C57BL/6J mice fed with a normal diet were served as control. After 4 weeks of intragastric administration, samples were harvested, and serum, aorta, heart, and liver tissues were isolated for subsequent experiments. Biochemical kits were used to detect serum lipid content in mice. Hematoxylin-eosin, Oil Red O and Masson staining were used to assess lesion severity, lipid deposition, and fibrous cap thickness. Transmission electron microscopy and immunofluorescence were used to analyze mitochondrial morphology and function. Real time quantitative PCR assay and Western blot were utilized to measure the expression levels of SIRT1, PGC-1α, Nrf1, and mitochondrial transcription factor A (TFAM) at both the mRNA and protein levels, along with the quantification of mitochondrial DNA (mtDNA) copy-number in mouse aortas. Results: After BBR intervention, BBRM and BBRH groups significantly reduced blood lipid levels in mice (P＜0.01), alleviated aortic plaque deposition, and improved mitochondrial damage (P＜0.05 or P＜0.01). Additionally, BBR significantly upregulated the mRNA and protein expressions of SIRT1, PGC-1α, Nrf1, and TFAM (P＜0.05 or P＜0.01). And the relative copy number of mtDNA increased in a dose-dependent manner (P＜0.01). In the BBRH+EX527 group, aortic lesions and mitochondrial damage were exacerbated, with concurrent decreases in mRNA and protein expression levels (P＜0.05 or P＜0.01). Conclusion: BBR promotes mitochondrial biogenesis, maintains mitochondrial function, and inhibits mitochondrial damage through the SIRT1/PGC-1α signaling pathway, thereby improving atherosclerosis.Keywords：atherosclerosis;berberine;mitochondrial biogenesis;SIRT1/PGC-1α signaling pathway26|0|0Updated：2026-11-13
- Abstract：Objective: To investigate the specific role and underlying mechanisms of individual herbs in Qingda Granule (QDG) in attenuating hypertension and inhibiting proliferation of vascular smooth muscle cells (VSMCs). Methods: Spontaneously hypertensive rats (SHRs) and angiotensin Ⅱ (AngⅡ)-stimulated VSMCs were treated with QDG or its individual herbs. SHRs were divided into groups using a completely randomized design: SHRs, valsartan (Val), QDG, Gastrodia elata Blume (Tianma, Gas), Uncaria rhynchophylla Miz. ex Havil. (Gouteng, Unc), Scutellaria baicalensis Georgi (Huangqin, Scu), and Nelumbo nucifera Gaertn (Lianzixin, Nel), 6 in each group. All treatments were administered via intragastric gavage once daily for 10 weeks. Vascular function and pathological changes were evaluated by ultrasonography and HE staining. The proliferation of VSMCs was assayed by cell counting kit-8, immunohistochemistry (IHC), and Western blot. RNA sequencing was performed to identify differentially expressed transcripts (DETs) in the abdominal aorta. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed to identify the key signaling pathways, and the expression of pathway-related proteins was subsequently verified by IHC and Western blot. Results: QDG and its individual herb treatments significantly attenuated the increase in pulse wave velocity and aortic wall thickness in SHRs. QDG inhibited the increased PCNA expression and cell viability in VSMCs. Unc, Scu, and Nel exhibited effects similar to QDG, while Gas did not show these effects. RNA sequencing analysis identified DETs in abdominal aortic tissues. KEGG analysis based on the DETs revealed that multiple common and unique signaling pathways were enriched. Among them, the MAPK pathway was enriched in the QDG, Unc, Scu, and Nel groups, but not in the Gas group, and the cAMP pathway was significantly enriched in all groups. IHC and Western blot analysis verified that compared with the SHR group, the QDG, Unc, Scu, and Nel groups inhibited MAPK pathway activation and promoted cAMP pathway activation in the abdominal aorta of SHR and Ang Ⅱ-stimulated A7R5s (P＜0.05). However, Gas only inhibited the activation of the p38 MAPK pathway and promoted the activation of the cAMP pathway (P＜0.05). Conclusions: The herbs in QDG exert significant antihypertensive effects by regulating common and unique pathways. Specifically, Unc, Scu, and Nel inhibit ERK and JNK pathway activation, which likely underlies QDG's suppression of VSMCs proliferation.Keywords：hypertension;vascular smooth muscle cells proliferation;Qingda Granule;compatibility of traditional Chinese herbal33|0|0Updated：2026-11-13
- Abstract：Objective: To explore the molecular mechanism of Xuefu Zhuyu Decoction (XFZYD) against myocardial fibrosis. Methods: The active components of XFZYD were identified by high performance liquid chromatography (HPLC). Network pharmacology, molecular docking, and affinity dot-mass spectrometry (AD-MS) were used to predict and validate the binding interaction between XFZYD components and copper transporter 1 (CTR1). Sixty male Kunming mice were randomly divided into 6 groups using a random number table. Control, isoproterenol hydrochloride (ISO), captopril, low-, medium-, and high-dose XFZYD (5.69, 11.38, and 22.76 g/kg) groups, with 10 mice in each group. Except the control group, mice received daily subcutaneous injection of ISO (10 mg/kg) for 28 d to induce myocardial fibrosis, concurrently treated with respective drugs by gavage. Cardiac function was assessed by echocardiography (ECG) and electrocardiography (UCG). Serum myocardial injury markers and transforming growth factor beta 1 (TGF-β1) were measured by a biochemical analyzer and enzyme-linked Immunosorbent assay (ELISA). Pathological changes and collagen deposition was observed using HE, Masson and sirius red staining methods. Copper content in cardiac tissue was determined by inductively coupled plasma mass spectrometry (ICP-MS), and protein expressions of collagen Ⅰ, Ⅲ, alpha-smooth muscle actin (α-SMA), lysyl oxidase (LOX), CTR1, copper chaperone for superoxide dismutase (CCS), and cytochrome c oxidase 17 (COX17) were detected by Western blot, immunohistochemistry, and immunofluorescence. In vitro, TGF-β1 (5 ng/mL)-stimulated NIH-3T3 fibroblasts were treated with XFZYD (60 mg/L), with or without CuCl2 (20 μmol/L) or SLC31A1 overexpression for 24 h, and the same indicators were evaluated. Results: HPLC identified 7 major components in XFZYD. Network pharmacology revealed that XFZYD targets copper metabolism related genes. Molecular docking showed strong binding affinities between the 7 compounds and CTR1, and AD-MS confirmed direct binding of paeoniflorin and amygdalin to CTR1. In vivo, XFZYD could ameliorate the collagen deposition, cardiac dysfunction, and elevated levels of collagen Ⅰ/Ⅲ, α-SMA, LOX, and copper content exhibited in ISO-induced myocardial fibrosis mice (P＜0.05 or P＜0.01). In vitro, XFZYD had the effects of suppressing copper overload and the upregulation of LOX, collagen Ⅰ/Ⅲ, and α-SMA in TGF β1 stimulated NIH-3T3 fibroblasts, whereas co-treatment with CuCl2 exacerbates these fibrotic responses and attenuates the protective effect of XFZYD (P＜0.05 or P＜0.01). XFZYD had the effect of partially reversing the enhanced copper accumulation, LOX activation, and collagen deposition induced by SLC31A1 (CTR1) overexpression in TGF β1 stimulated fibroblasts, and SLC31A1 overexpression reduces its efficacy (P＜0.05 or P＜0.01). Conclusions: XFZYD exerted a protective effect against ISO-induced myocardial fibrosis. The mechanism may be related to regulating the CTR1- copper-LOX axis, thereby reducing excessive collagen deposition and cross-linking in cardiac fibroblasts.Keywords：myocardial fibrosis;Xuefu Zhuyu Decoction;copper transporter 1;copper;lysyl oxidase;Chinese medicine31|2|0Updated：2026-11-13
- Abstract：Objective: To investigate the therapeutic mechanisms of Eucommia ulmoides Oliv. (EC) in a collageninduced arthritis (CIA) rat model. Methods: The CIA model was established by immunizing rats with type Ⅱ collagen. Wistar rats were assigned to the normal group (n=6), and the remaining model rats were further divided by body weight into the CIA model, EC, and Iguratimod (IGU) positive control groups (n=6 per group). EC (4 g/kg per day) and IGU (4.5 mg/kg daily) was administered orally for 4 weeks. Arthritis severity was evaluated by measuring hind paw volume. Histopathological analysis of ankle joints was performed using hematoxylin and eosin (HE) and safranin O/fast green. Serum levels of procollagen type Ⅰ N-terminal propeptide (PINP), cross-linked carboxy-terminal telopeptide of type Ⅰ collagen (ICTP), osteocalcin (BGP), β-crosslaps (β-CTX), tumor necrosis factor (TNF-α), interleukin (IL)-1β, and CTNNB1 (β-catenin) were measured by ELISA. Serum nitric oxide (NO) levels were measured using a nitrate reductase assay. Transcriptomic sequencing and RT-qPCR were performed to assess mRNA expression, and Western blot was used to assess protein expression of Wnt2 and β-catenin in the spleen. Results: Compared with the CIA group, EC significantly alleviated arthritis severity and paw swelling (P＜0.05) and reduced synovial inflammation and cartilage damage. Serum analysis showed that EC decreased TNF-α, IL-1β, NO, ICTP, and β-CTX, while increasing PINP and BGP (P＜0.05 or P＜0.01), and also reduced CTNNB1 (P＜0.01) compared with the CIA group. In the spleen, EC reduced mRNA expressions of IL-1β, IL-6, and TNF-α (P＜0.05 or P＜0.01), upregulated IL-10, and decreased β-catenin protein (P＜0.05); Wnt2 mRNA showed a non-significant downward trend compared with the CIA group. In the ankle joints, EC significantly reduced mRNA expressions of Wnt2 and β-catenin (P＜0.05 or P＜0.01). Conclusion: EC may alleviate inflammation and bone destruction in RA by regulating the Wnt/β-catenin signaling pathway, suggesting its potential as a therapeutic agent for RA.Keywords：Eucommia ulmoides Oliv.;Chinese medicine;rheumatoid arthritis;collagen-induced arthritis;Wnt/β-catenin signaling pathway22|0|0Updated：2026-11-13
- Abstract：Objective: To elucidate whether Danggui Sini Decoction (DGSD) relieves sciatica by downregulating transient receptor potential (TRP) channels involved in peripheral sensitization. Methods: After conducting chronic constriction injury of sciatic nerve (CCI) operation, 32 SD rats, randomly assigned to the sham, CCI 7d, CCI 14d, and CCI 21d groups (n=8 per group), were used to observe the course of sciatica. mRNA sequencing of dorsal root ganglia (DRG) was conducted on rats in the sham and CCI 21d groups. Another 32 rats were divided into the sham, CCI, mecobalamin, and DGSD groups, 8 in each group. mRNA sequencing analysis and single-cell RNA-sequencing (scRNA-seq) data analysis were conducted. Behavioural tests were conducted to evaluate the therapeutic effects of DGSD. The levels of TRP vanilloid (TRPV)1-4, TRP ankyrin 1 (TRPA1), TRP melastatin 8 (TRPM8), Ras homolog family member A (RhoA), and phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) were measured via Western blot, and the serum levels of C-C motif chemokine ligand 2 and 5 (CCL2, CCL5), substance P (SP), and prostaglandin E2 (PGE2) were conducted via ELISA. Results: scRNA-seq and mRNA sequencing analysis revealed that inflammatory mediator regulation of TRP channels played a role in the development of sciatica. CCI rats exhibited cold hyperalgesia from day 4 to 21, increased the DRG protein expression levels of TRP channels, including TRPV1-4, TRPA1, TRPM8, RhoA, p-p38MAPK, CCL2, CCL5, SP, and PGE2. Treatment with DGSD decreased the serum levels of CCL2, CCL5, SP, and PGE2, and reduced the levels of RhoA, p-p38MAPK, TRPV1-4, TRPA1, and TRPM8 in DRG (P＜0.05). Conclusion: CCI increased the levels of TRP channels and inflammatory factors, inducing cold hyperalgesia, whereas DGSD relieved pain via inhibiting peripheral sensitization to relieve cold hyperalgesia by reducing the inflammatory factors and TRP.Keywords：peripheral sensitization;transient receptor potential channels;sciatica;Danggui Sini Decoction;chronic constriction injury of the sciatic nerve;Chinese medicine24|0|0Updated：2026-11-13
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Herbal and Batanical Review
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