The pathogenesis of metabolic dysfunction-associated steatotic liver disease （MASLD） is fundamentally rooted in spleen deficiency and is closely associated with phlegm turbidity， damp-heat and blood stasis. Clinically， liver constraint with spleen deficiency and internal retention of damp turbidity represent the predominant traditional Chinese medicine （TCM） syndrome patterns. Researches have indicated intrinsic connections between the syndrome patterns and biological indicators such as gut microbiota and metabolic profiles. Regarding treatment， classical famous formulas， modern empirical formulas， and newly developed TCM drugs show positive effects in regulating glucose and lipid metabolism， improving insulin resistance， and alleviating metabolic inflammation， exhibiting multi-target mechanisms of action； acupuncture and other external therapies also provide adjunctive value. Nevertheless， current researches still have limitations such as the lack of high-quality clinical evidence and insufficient systematic elucidation of the uncerlying mechanisms. Future efforts should focus on conducting high-quality TCM clinical trials with hard endpoint outcomes such as hepatic histology outcomes， and utilizing modern technologies like multi-omics to elucidate TCM's mechanisms of action， thereby advancing the position of TCM as a first-line therapeutic strategy for MASLD.

ObjectiveThis study aims to explore the effect of Feiyanning granules on ferroptosis in lung cancer cells and its regulatory function within the nuclear transcription factor E₂-related factor 2 （Nrf2）/mouse solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） signaling pathway. MethodsThe cell counting kit-8 （CCK-8） method was used to detect the effect of Feiyanning granule on the proliferation of A549 lung cancer cells. A549 lung cancer cells were categorized into a blank group， a ferroptosis inhibitor-1 （Fer-1） group （10 μmol·L^-1）， a Feiyanning granules （600 mg·L^-1） group， and a Feiyanning granules + Fer-1 group. After 48 hours of intervention， the activity and morphology of the cells were observed. The CCK-8 method was employed to measure cell viability. Biochemical assays were carried out to measure the levels of reactive oxygen species （ROS）， malondialdehyde （MDA）， glutathione （GSH）， and ferrous ions （Fe²⁺） in A549 cells. Western blot was utilized to evaluate the expression levels of Kelch-like ECH-associated protein 1 （Keap1）， Nrf2， SLC7A11， and GPX4 proteins. A549 lung cancer cells were categorized into a blank group and a Feiyanning Granule group （600 mg·L^-1）， and mitochondrial morphology was examined via transmission electron microscopy （TEM）. ResultsAfter the intervention of Feiyaning granules， the proliferation of A549 cells was significantly inhibited in a concentration-dependent manner compared with that in the blank group （P<0.01）. Compared with the blank group， the Feiyanning granules group exerted an significantly inhibitory effect on the viability of lung cancer cells （P<0.01）. Compared with that in the Feiyanning granules group， the cell viability in the Feiyanning granules +Fer-1 group was obviously restored （P<0.05）. Compared with the blank group， the Feiyanning Granule group showed a significant increase in the levels of ROS， MDA， and Fe²⁺ （P<0.01）， a significant decrease in the GSH level （P<0.01）， and facilitated ferroptosis. Compared with the blank group， the Feiyanning granules group showed significantly decreased expression of Nrf2， SLC7A11， and GPX4 proteins and enhanced expression of Keap1 （P<0.01）. Compared with those in the Feiyanning Granule group， the protein levels of Nrf2， SLC7A11， and GPX4 increased significantly （P<0.01）， and the expression of Keap1 decreased significantly in the Feiyanning granules + Fer-1 group （P<0.01）. Compared with the blank group， the Feiyaning granules group exhibited reduced mitochondrial size and increased matrix electron density. ConclusionFeiyanning granules can induce ferroptosis in lung cancer cells， and its underlying mechanism might be associated with the inhibition of the Nrf2/SLC7A11/GPX4 signaling pathway.

Objective To explore the molecular mechanism of Jianfu mixture in the treatment of erectile dysfunction （ED） by network pharmacology and molecular docking techniques, and validate its core targets and mechanisms through in vitro experiments. Methods The active components and corresponding molecular targets of Jianfu mixture were searched by searching TCMSP and Batman-TCM databases, and the disease targets of ED were searched by using GeneCards database. Find the intersection of drug ingredient target and disease target. The interaction between intersected targets was described and analyzed by String database, and the analysis results were visualized by Cytoscape software to determine the core target and the corresponding active components. GO functional enrichment analysis and KEGG pathway enrichment analysis were performed for intersection targets; the core target within the intersection were found through MCODE plug-in on Cytoscape software and molecular docking was performed with the corresponding active ingredients. An endothelial dysfunction model was established by transfecting HUVECs with si-eNOS. Intervene with different concentrations of the Jianfu mixture for the model cells for 24 h. QPCR was used to detect mRNA expression of core targets （MAPK1, MAPK3, JUN, ESR1, MAPK8）; Western blot was used to analyze protein expression （eNOS, JUN, p-JUN, MAPK, p-MAPK） and phosphorylation levels. Results 144 effective active components and 168 active components target-disease targe intersection of Jianfu mixture were obtained. GO analysis revealed 200 5 biological processes, 151 molecular functions, and 63 cellular components. KEGG analysis yielded 181 pathways. 5 core targets including MAPK1, MAPK3, JUN, ESR1 and MAPK8 were screened out. The active components such as β-sitosterol, kaempferol, astapterocarpan had good binding affinity with the core target. In vitro experiments confirmed successful construction of the endothelial dysfunction model （eNOS expression significantly decreased after si-eNOS transfection）. Jianfu mixture dose-dependently inhibited mRNA expression of MAPK1, MAPK3, JUN, ESR1, and MAPK8. Additionally, it reduced phosphorylation levels of JUN and MAPK, indicating inhibition of the JNK/c-Jun and ERK/MAPK signaling pathways to improve endothelial function. Conclusion Jianfu mixture treats ED by suppressing abnormal activation of multi-target signaling pathways （MAPK/JUN/ESR1）, reducing endothelial apoptosis, and promoting NO synthesis. This mechanism aligns with the traditional Chinese medicine principle of “activating blood circulation, resolving stasis, tonifying Qi, and strengthening cardiovascular function.” The study provided molecular-level evidence for the therapeutic efficacy of Jianfu mixture in ED management.

Objective To explore the molecular mechanism of Jianfu mixture in the treatment of erectile dysfunction （ED） by network pharmacology and molecular docking techniques, and validate its core targets and mechanisms through in vitro experiments. Methods The active components and corresponding molecular targets of Jianfu mixture were searched by searching TCMSP and Batman-TCM databases, and the disease targets of ED were searched by using GeneCards database. Find the intersection of drug ingredient target and disease target. The interaction between intersected targets was described and analyzed by String database, and the analysis results were visualized by Cytoscape software to determine the core target and the corresponding active components. GO functional enrichment analysis and KEGG pathway enrichment analysis were performed for intersection targets; the core target within the intersection were found through MCODE plug-in on Cytoscape software and molecular docking was performed with the corresponding active ingredients. An endothelial dysfunction model was established by transfecting HUVECs with si-eNOS. Intervene with different concentrations of the Jianfu mixture for the model cells for 24 h. QPCR was used to detect mRNA expression of core targets （MAPK1, MAPK3, JUN, ESR1, MAPK8）; Western blot was used to analyze protein expression （eNOS, JUN, p-JUN, MAPK, p-MAPK） and phosphorylation levels. Results 144 effective active components and 168 active components target-disease targe intersection of Jianfu mixture were obtained. GO analysis revealed 200 5 biological processes, 151 molecular functions, and 63 cellular components. KEGG analysis yielded 181 pathways. 5 core targets including MAPK1, MAPK3, JUN, ESR1 and MAPK8 were screened out. The active components such as β-sitosterol, kaempferol, astapterocarpan had good binding affinity with the core target. In vitro experiments confirmed successful construction of the endothelial dysfunction model （eNOS expression significantly decreased after si-eNOS transfection）. Jianfu mixture dose-dependently inhibited mRNA expression of MAPK1, MAPK3, JUN, ESR1, and MAPK8. Additionally, it reduced phosphorylation levels of JUN and MAPK, indicating inhibition of the JNK/c-Jun and ERK/MAPK signaling pathways to improve endothelial function. Conclusion Jianfu mixture treats ED by suppressing abnormal activation of multi-target signaling pathways （MAPK/JUN/ESR1）, reducing endothelial apoptosis, and promoting NO synthesis. This mechanism aligns with the traditional Chinese medicine principle of “activating blood circulation, resolving stasis, tonifying Qi, and strengthening cardiovascular function.” The study provided molecular-level evidence for the therapeutic efficacy of Jianfu mixture in ED management.

ObjectiveTo investigate the molecular mechanism by which Feiyanning formula（FYN） regulated exosomal miR-328 to suppress the invasion and metastasis of lung cancer. MethodsIn vitro models using low-metastatic 95C and high-metastatic 95D lung cancer cell lines， along with isolated exosomes， were established. Initially， 95C and 95D cells were cultured， and exosomes were isolated from their supernatants. The exosomes were identified using transmission electron microscopy （TEM）， nanoparticle tracking analysis （NTA）， and Western blot. Exosome uptake assays confirmed that both 95C and 95D cells could internalize exosomes derived from lung cancer patients' plasma. Cell counting kit-8 （CCK-8） assays were performed to assess the inhibitory effects of FYN （0， 0.1， 0.2， 0.4， 0.8， 1.6， 3.2， 6.4 g·L^-1） on 95C and 95D cell proliferation. Subsequent experiments were divided into three groups of control， low-dose FYN （1 g·L^-1）， and high-dose FYN （2 g·L^-1） groups. Wound-healing and Transwell assays were used to evaluate the inhibitory effects of FYN on the migration and invasion of 95C and 95D cells. Western blot was employed to detect the protein expression levels of Janus kinase 2 （JAK2）， signal transducer and activator of transcription 3 （STAT3）， cellular oncogene Fos （c-Fos）， and nuclear factor of activated T cells 1 （NFATc1）. The mRNA expression of miR-328 was measured by Real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsLung cancer plasma-derived exosomes （EXO） enhanced the migration， invasion， and miR-328 expression levels in 95C and 95D cells （P<0.05， P<0.01）. FYN inhibited the proliferation， invasion， and metastasis of 95C and 95D cells in a dose-dependent manner （P<0.01）， with more pronounced effects on 95C cells. Additionally， FYN downregulated exosomal miR-328 expression and suppressed the protein levels of JAK2， STAT3， and its downstream target genes c-Fos and NFATc1 （P<0.01）. ConclusionFYN may inhibit lung cancer metastasis by downregulating exosomal miR-328 expression， potentially through the STAT3/c-Fos/NFATc1 signaling pathway. Further studies are warranted to elucidate its detailed mechanisms and facilitate clinical application， providing insights into traditional Chinese medicine-based strategies for lung cancer treatment.

Cremastrae Pseudobulbus Pleiones Pseudobulbus is a Chinese medicinal material used for clearing heat， detoxicifying， resolving phlegm， and dissipating nodules. It is derived from Cremastra appendiculata， Pleione bulbocodioides， or Pleione yunnanensis， as recorded in the 2025 edition of the Pharmacopoeia of the People′s Republic of China， with the former known as Maocigu and the latter two known as Bingqiuzi. Current antitumor studies mainly focus on polysaccharides， water-extracted alcohol-precipitated fractions， and purified extracts of C. appendiculata. Structurally characterized glucomannans suppress breast and liver tumor xenografts and exhibit immunomodulatory effects. The water-extracted alcohol-precipitated fractions inhibit tumor angiogenesis in hepatoma-bearing mice. A purified C. appendiculata extract standardized to five phenanthrene and bibenzyl constituents induces mitochondrial apoptosis in hepatocellular carcinoma cells. Reported pharmacological effects involve cell-cycle regulation， apoptosis， epithelial-mesenchymal transition， angiogenesis， autophagy， and the tumor immune microenvironment， with phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR）， Wnt/β-catenin， and Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathways being the major mechanism links. Quality evaluation of Cremastrae Pseudobulbus Pleiones Pseudobulbus has progressed from single-marker assays to an integrated approach involving botanical authentication， chromatographic fingerprinting， multicomponent analysis， and evaluation of associations between blood-absorbed constituents and antitumor effects. Militarine and dactylorhin A can be used for botanical identification and batch evaluation， and in vivo exposure data from related orchids are concentrated on militarine. Quantitative associations between these constituents and antitumor effects remain to be established. Clinical evidence mainly focuses on formula-based applications and expert experience. Comparative antitumor data in hepatoma models are available for the commercial specifications of Maocigu and Bingqiuzi， whereas parallel evaluations of pharmacological effects， safety windows， and drug interactions among the three official botanical origins remain insufficient. The major limitations are the incomplete standardization of botanical origins and preparations and the lack of quantitative links among quality markers， systemic exposure， antitumor effects， and toxicity endpoints， which constrain reproducible pharmacological evaluation and clinical translation of Cremastrae Pseudobulbus/Pleiones Pseudobulbus.

ObjectiveTo investigate the neuroprotective effects of Tiaoseng decoction on a perimenopausal depression （PMD） rat model and to examine its regulatory influence on the estrogen receptor β （ERβ）/monoamine oxidase A （MAOA）/c-Jun N-terminal kinase （JNK） signaling pathway， thereby elucidating its potential mechanisms of action. MethodsForty-eight female Sprague-Dawley （SD） rats were divided into a sham group， a model group， a 17β-estradiol （E₂） group （2.5 × 10^-5 g·kg^-1）， and low-， medium-， and high-dose Tiaoseng decoction groups （9.69， 19.37， 38.74 g·kg^-1） by using a random number table method， with eight rats in each group. The PMD model was replicated using ovariectomy （OVX） combined with chronic unpredictable mild stress （CUMS） and was treated continuously with 17β-E₂ and different doses of Tiaoseng decoction for 28 d， once a day. Depressive-like behaviors were assessed using the sucrose preference test， open-field test， and forced swim test. Histopathological changes in the prefrontal cortex were examined using hematoxylin-eosin （HE） and Nissl staining. Enzyme-linked immunosorbent assay （ELISA） was performed to measure serum levels of E₂， luteinizing hormone （LH）， and follicle-stimulating hormone （FSH）， as well as reactive oxygen species （ROS）， malondialdehyde （MDA）， and superoxide dismutase （SOD） levels in the prefrontal cortex. Mitochondrial ultrastructure of prefrontal cortex neurons was observed via transmission electron microscopy. Terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） was used to detect neuronal apoptosis in the prefrontal cortex. Immunohistochemistry （IHC） was applied to analyze the protein expression of brain-derived neurotrophic factor （BDNF）， postsynaptic density protein95 （PSD95）， and synaptophysin （SYP） in the prefrontal cortex. Immunofluorescence （IF） was conducted to evaluate the average fluorescence intensity of ERβ and MAOA in the prefrontal cortex. Western blot and real-time quantitative polymerase chain reaction （Real-time PCR） were used to determine the protein and mRNA expression levels of key molecules in the ERβ/MAOA/JNK signaling pathway in the prefrontal cortex. ResultsCompared with the sham group， the model group had significantly reduced sugar-water preference index， total distance traveled， average speed， and activity time in the central region in the open field experiment， E₂ content， and SOD content （P<0.01） and significantly reduced BDNF， PSD95， SYP， and ERβ expression and B-cell lymphoma-2 （Bcl-2）/Bcl-2-associated X protein （Bax） ratio （P<0.01）. Additionally， the model group exhibited severe histopathological damage， disrupted mitochondrial structure， cristae disappearance or fracture， swelling， and deformation in the prefrontal lobe. The immobilization time of forced swimming， TUNEL positivity， LH， FSH， MDA， ROS， MAOA， Caspase-3， p-JNK/JNK， and p-c-Jun/c-Jun were significantly increased in the model group compared with the sham group （P<0.01）. Compared with the model group， the low-， medium-， and high-dose Tiaoseng decoction groups and the 17β-E₂ group had increased sugar-water preference index， total distance traveled， average speed， and activity time in the central region in the open-field test， E₂ content， and SOD content （P<0.05， P<0.01） and elevated BDNF， PSD95， SYP， and ERβ expression and Bcl-2/Bax ratio （P<0.05， P<0.01）. In addition， histopathological damage to the prefrontal lobe was improved to different degrees， and mitochondrial structure was gradually repaired. The immobilization time of forced swimming， TUNEL positivity， LH， FSH， MDA， ROS， MAOA， Caspase-3， p-JNK/JNK and p-c-Jun/c-Jun were significantly reduced in the low-， medium-， and high-dose Tiaoseng decoction groups and the 17β-E₂ group compared with the model group （P<0.05， P<0.01）. ConclusionTiaoseng decoction has significant neuroprotective effects on PMD model rats， which can alleviate perimenopausal depressive disorder by inhibiting oxidative stress， attenuating neuronal apoptosis， and restore synaptic plasticity via ERβ/MAOA/JNK signaling pathway regulation.

ObjectiveTo explore the mechanism of the anti-cancer compound formula Feiyanning in inhibiting epithelial-mesenchymal transition （EMT） and invasion and metastasis of non-small cell lung cancer （NSCLC）. MethodsCell proliferation and activity were assessed using the cell counting kit-8（CCK-8） assay to evaluate the effect of Feiyanning on the proliferation of A549 and H1299 cells. Wound healing and Transwell assays were conducted to examine Feiyanning's impact on the metastasis of A549 and H1299 cells. The effects of Feiyanning on EMT and the transforming growth factor-β₁ （TGF-β₁）/Smad signaling pathway proteins in A549 and H1299 cells were detected by Western blot. Exogenous TGF-β₁ was used to induce EMT in A549 and H1299 cells. The effects of Feiyanning on TGF-β₁-induced NSCLC cell metastasis， EMT， and the TGF-β₁/Smad pathway proteins were assessed by wound healing assay， Transwell assay， and Western blot. In vivo， an A549 lung metastasis model was established via tail vein injection in nude mice. A total of 28 SPF male nude mice were randomly divided into four groups： Model （NC） group， Feiyanning low-dose （FYN1） group， Feiyanning high-dose （FYN2） group， and the positive control group （TGF-β receptor kinase inhibitor SB431542 group）. The corresponding interventions were performed. After 40 days， the mice were euthanized， and lung metastases were analyzed. The expression of E-cadherin， N-cadherin， p-Smad2， and p-Smad3 in each group was detected by immunohistochemistry （IHC）. ResultsAfter Feiyanning intervention， compared to the blank group， Feiyanning inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner （P<0.01）. The metastasis ability of Feiyanning-treated cells was significantly decreased compared to the blank group （P<0.01）. The expression of EMT marker proteins N-cadherin and zinc finger transcription factors （Zeb1， Snail， Slug） was significantly reduced in the Feiyanning groups compared to the blank group （P<0.05， P<0.01）. The expression of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ， key proteins in the TGF-β₁/Smad signaling pathway， was also significantly decreased （P<0.01）. In the TGF-β₁-induced EMT model， compared to the TGF-β₁ group， the cell metastasis ability in the Feiyanning groups was reduced （P<0.01）， and the expression levels of N-cadherin， Zeb1， Snail， and Slug were significantly lower （P<0.01）. The expression levels of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ were also significantly reduced （P<0.01）. In vivo results showed that compared to the model group， the number of lung metastases in the FYN1， FYN2， and SB431542 groups was reduced （P<0.01）， and the range of cell infiltration was narrowed. Immunohistochemical results showed that compared to the model group， the expression of E-cadherin in the FYN1， FYN2， and SB431542 groups was increased （P<0.01）， the expression of N-cadherin decreased （P<0.05， P<0.01）， and the expression of p-Smad2 and p-Smad3， key proteins of the TGF-β₁/Smad pathway， was reduced （P<0.01）. ConclusionFeiyanning inhibits the invasion and metastasis of NSCLC cells and EMT. The mechanism is related to the inhibition of TGF-β₁/Smad signaling pathway.

ObjectiveTo explore the mechanism of the anti-cancer compound formula Feiyanning in inhibiting epithelial-mesenchymal transition （EMT） and invasion and metastasis of non-small cell lung cancer （NSCLC）. MethodsCell proliferation and activity were assessed using the cell counting kit-8（CCK-8） assay to evaluate the effect of Feiyanning on the proliferation of A549 and H1299 cells. Wound healing and Transwell assays were conducted to examine Feiyanning's impact on the metastasis of A549 and H1299 cells. The effects of Feiyanning on EMT and the transforming growth factor-β₁ （TGF-β₁）/Smad signaling pathway proteins in A549 and H1299 cells were detected by Western blot. Exogenous TGF-β₁ was used to induce EMT in A549 and H1299 cells. The effects of Feiyanning on TGF-β₁-induced NSCLC cell metastasis， EMT， and the TGF-β₁/Smad pathway proteins were assessed by wound healing assay， Transwell assay， and Western blot. In vivo， an A549 lung metastasis model was established via tail vein injection in nude mice. A total of 28 SPF male nude mice were randomly divided into four groups： Model （NC） group， Feiyanning low-dose （FYN1） group， Feiyanning high-dose （FYN2） group， and the positive control group （TGF-β receptor kinase inhibitor SB431542 group）. The corresponding interventions were performed. After 40 days， the mice were euthanized， and lung metastases were analyzed. The expression of E-cadherin， N-cadherin， p-Smad2， and p-Smad3 in each group was detected by immunohistochemistry （IHC）. ResultsAfter Feiyanning intervention， compared to the blank group， Feiyanning inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner （P<0.01）. The metastasis ability of Feiyanning-treated cells was significantly decreased compared to the blank group （P<0.01）. The expression of EMT marker proteins N-cadherin and zinc finger transcription factors （Zeb1， Snail， Slug） was significantly reduced in the Feiyanning groups compared to the blank group （P<0.05， P<0.01）. The expression of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ， key proteins in the TGF-β₁/Smad signaling pathway， was also significantly decreased （P<0.01）. In the TGF-β₁-induced EMT model， compared to the TGF-β₁ group， the cell metastasis ability in the Feiyanning groups was reduced （P<0.01）， and the expression levels of N-cadherin， Zeb1， Snail， and Slug were significantly lower （P<0.01）. The expression levels of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ were also significantly reduced （P<0.01）. In vivo results showed that compared to the model group， the number of lung metastases in the FYN1， FYN2， and SB431542 groups was reduced （P<0.01）， and the range of cell infiltration was narrowed. Immunohistochemical results showed that compared to the model group， the expression of E-cadherin in the FYN1， FYN2， and SB431542 groups was increased （P<0.01）， the expression of N-cadherin decreased （P<0.05， P<0.01）， and the expression of p-Smad2 and p-Smad3， key proteins of the TGF-β₁/Smad pathway， was reduced （P<0.01）. ConclusionFeiyanning inhibits the invasion and metastasis of NSCLC cells and EMT. The mechanism is related to the inhibition of TGF-β₁/Smad signaling pathway.

OBJECTIVE: To explore the efficacy and safety of Juan Bi Pill (JBP) in treatment of active rheumatoid arthritis (RA). METHODS: From February 2017 to May 2018, 115 participants from 4 centers were randomly divided into JBP group (57 cases) and placebo group (58 cases) in a 1:1 ratio using a random number table method. Participants received a dose of JBP (4 g, twice a day, orally) combined with methotrexate (MTX, 10 mg per week) or placebo (4 g, twice a day, orally) combined with MTX for 12 weeks. Participants were required with follow-up visits at 24 and 48 weeks, attending 7 assessment visits. Participants were undergo disease activity assessment 7 times (at baseline and 2, 4, 8, 12, 24, 48 weeks) and safety assessments 6 times (at baseline and 4, 8, 12, 24, 48 weeks). The primary endpoint was 28-joint Disease Activity Score (DAS28-ESR and DAS28-CRP). The secondary endpoints included American College of Rheumatology (ACR) criteria for 20% and 50% improvement (ACR20/50), Health Assessment Questionnaire Disability Index (HAQ-DI), clinical disease activity index (CDAI), visual analog scale (VAS), Short Form-36 (SF-36) score, Medial Outcomes Study (MOS) sleep scale score, serum erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), tender joint count, swollen joint count, and morning stiffness. The adverse reactions were observed during the treatment. RESULTS: After 12 weeks of treatment, DAS28-ESR and DAS28-CRP scores in both groups were lower than before treatment (both P<0.01), while the remission rate of DAS28-ESR and DAS28-CRP and low disease activity of JBP group were higher than those in the placebo group (both P<0.01). JBP demonstrated better efficacy on ACR20 and ACR50 compliance rate at 12 and 48 weeks comparing to placebo (all P<0.05). The CDAI and HAQ-DI score, pain VAS and global VAS change of RA patients and physicians, the serum ESR and CRP levels, and the number of tenderness and swelling joints were lower than before treatment at 4, 8, 12, 24, 48 weeks in both groups (P<0.05 or P<0.01), while the reduction of above indices in the JBP group was more obvious than those in the placebo group at 12 weeks (ESR and CRP, both P<0.05) or at 12 and 48 weeks (all P<0.01). There was no difference in adverse reactions between the 2 groups during treatment (P=0.75). CONCLUSION JBP combined with MTX could effectively reduce disease activity in patients with RA in active stage, reduce the symptoms of arthritis, and improve the quality of life, while ensuring safety, reliability, and fewer adverse effects. (Trial Registration: ClinicalTrials.gov, No. NCT02885597).
Humans ; Arthritis, Rheumatoid/drug therapy* ; Methotrexate/adverse effects* ; Female ; Double-Blind Method ; Male ; Middle Aged ; Treatment Outcome ; Drugs, Chinese Herbal/adverse effects* ; Drug Therapy, Combination ; Adult ; Antirheumatic Agents/adverse effects* ; Aged