ObjectiveBased on the multidimensional correlation analysis framework of "disease， syndrome， formula， and medicine"， this study aims to systematically elucidate the regulatory effects of effective components in Qiangjing tablet on testosterone synthesis pathways in testicular Leydig cells under oxidative stress， providing a theoretical basis for the treatment of male infertility with traditional Chinese medicine and modern research on compounds. MethodsDisease targets for male infertility were obtained from The Human Gene Database （GeneCards， score ≥20）， the Comparative Toxicogenomics Database （CTD， score ≥150）， DrugBank （score ≥0.2）， and DisGeNET （score ≥0.2）. Targets related to the syndrome of kidney deficiency and blood stasis were acquired from the traditional Chinese medicine syndrome association database SymMap. Components of Qiangjing tablet were retrieved based on The Encyclopedia of Traditional Chinese Medicine （ETCM） database and the Integrative Pharmacology-based Research Platform of Traditional Chinese Medicine （TCMIP）， and they were screened according to a quantitative estimate of drug-likeness （QED ≥ 0.49） and a target confidence index>0.8. Intersecting targets were taken to construct a protein-protein interaction （PPI） network using the STRING database. The network was visualized with Cytoscape software and subjected to the functional annotation of gene ontology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） pathway enrichment analysis. Quality markers （Q-markers） were predicted via the ADMETlab 2.0 platform based on Lipinski's rule， Pfizer's rule， GSK's rule， and the Golden Triangle. For experimental validation， rats' testicular Leydig cells were used. Exosomes were extracted and loaded with active components via the ultrasonic method. Exosome concentration was determined using a BCA protein quantification kit. Morphology was observed using a transmission electron microscope. The particle size was analyzed with a particle size analyzer. The surface marker proteins such as cluster of differentiation 9 （CD9）， cluster of differentiation 63 （CD63）， and cluster of differentiation 81 （CD81） were identified by Western blot， and drug loading capacity was measured by high-performance liquid chromatography （HPLC）. An oxidative stress model was induced by alpha， alpha'-azodiisobutyramidine dihydrochloride （AAPH）， and Leydig cells were divided into the following groups： A control group， an AAPH group， a quercetin group （Que group）， an exosome group （Exo group）， and a QUE-loaded Exo group （Que-Exo group）. The cell viability was detected using the 3-（4，5-dimethylthiazol-2-yl）-2，5-diphenyltetrazolium bromide （MTT） thiazolyl blue assay. The reactive oxygen species （ROS） levels and mitochondrial membrane potential were measured by flow cytometry. The levels of oxidative indicators， including malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione peroxidase （GSH-Px）， catalase （CAT）， and testosterone （T）， were detected by enzyme-linked immunosorbent assay （ELISA）. The expressions of steroidogenic enzymes such as cytochrome p450 family 11 subfamily a member 1 （CYP11A1）， hydroxy-delta-5-steroid dehydrogenase， 3 beta- and steroid delta-isomerase 1 （HSD3B1）， and hydroxysteroid 17-beta dehydrogenase 3 （HSD17B3）， regulatory factors such as steroidogenic factor 1 （SF-1） and steroidogenic acute regulatory protein （StAR）， and miR-145-5p content， were detected by Western blot and real-time polymerse chain reaction （Real-time PCR）. ResultsNetwork pharmacology analysis reveals that the main active components of Qiangjing tablet for intervening in male infertility with kidney deficiency and blood stasis syndrome were Que， luteolin， etc.， with the core mechanism involving pathways such as steroid hormone biosynthesis. Experimental results show that compared with the control group， the AAPH group exhibits significantly reduced cell viability （P<0.01）， decreased mitochondrial membrane potential （P<0.01）， significantly elevated levels of ROS， MDA， and miR-145-5p （P<0.01）， significantly reduced activities of SOD， GSH-Px， and CAT， as well as reduced testosterone content （P<0.01）， and significantly downregulated protein and mRNA expressions of steroidogenic enzymes， SF-1， and StAR （P<0.01）. The above indicators were reversed in the Que and Que-Exo groups （P<0.05）. Compared with the Que group， the Que-Exo group showed more significant effects in enhancing cell viability， mitochondrial membrane potential， testosterone level， antioxidant enzyme activities， and expressions of key molecules in the steroidogenic pathway （P<0.05）. ConclusionThis study demonstrates that Que， an active component of Qiangjing tablet， inhibits oxidative stress reaction， improves mitochondrial function in Leydig cells， upregulates steroidogenic enzyme expression， and restores testosterone production. As a carrier for Que， Exo enhance its stability， delivery efficiency， and biological effect. Additionally， miR-145-5p may be closely associated with testosterone synthesis， though its precise molecular mechanism requires further exploration. By integrating traditional Chinese medicine compounds with modern scientific technology， this research expands the paths for the modernized research of traditional Chinese medicine and opens a novel therapeutic direction with translational potential for clinical intervention of male infertility.

Objective:To investigate the application of cardiac magnetic resonance (CMR) quantitative techniques in evaluating myocardial involvement differences between new onset and longstanding systemic lupus erythematosus (SLE) patients.Methods:From August 2020 to April 2023, 14 new onset and 15 longstanding SLE patients treated at the First Affiliated Hospital of Anhui Medical University were prospectively included as the study group. Additionally, 18 age-, gender-, body surface area-, and body mass index-matched healthy volunteers were included as the control group. Clinical baseline data, electrocardiograms, and CMR results including left ventricular ejection fraction (LVEF), left ventricular end-systolic volume index (LVESVI), left ventricular end-diastolic volume index (LVEDVI), cardiac index (CI), left ventricular stroke volume index (LVSVI), left ventricular mass index (LVMI), myocardial strain, native T 1 values, and T 2 values were collected. One-way analysis of variance (ANOVA) or Kruskal-Wallis H test was used to compare the quantitative parameters among the three groups. Bonferroni correction was applied for pairwise group comparisons. Results:The native T 1 values [1 114.50 (1 089.33, 1 150.39) ms, 1 085.32 (1 051.31, 1 129.75) ms] and T 2 values [(55.9±3.4) ms, (53.3±1.5) ms] of new onset and longstanding SLE patients were higher than those of the healthy control group [native T 1 values 1052.62 (1024.75, 1077.59) ms, H=17.72, P<0.001; T 2 values (51.2±1.3) ms, F=18.70, P<0.001]. The T 2 values of the new onset SLE group was higher than that of the longstanding SLE group ( P<0.05). The LVEDVI[86.87 (80.80, 93.55) ml/m 2], LVSVI [54.63 (50.42, 59.03) ml/m 2], and LVMI [48.39 (41.65, 53.26) g/m 2] of the new onset SLE group were higher than those of the control group [LVEDVI: 71.11 (65.80, 81.28) ml/m 2, Z=3.02, P=0.003; LVSVI: 42.17 (40.36, 51.33) ml/m 2, Z=2.76, P=0.006; LVMI: 38.48 (35.22, 43.83) g/m 2, Z=3.10, P=0.002]. The LVEDVI and LVSVI of the new onset SLE group were also higher than those of the longstanding SLE group [LVEDVI: 73.30 (69.87, 84.71) ml/m 2, Z=1.97, P=0.048; LVSVI: 45.53 (42.28, 50.98) ml/m 2, Z=2.34, P=0.020]. Conclusion:Myocardial involvement is more severe in new onset SLE patients, whereas acute myocardial injury is alleviated in longstanding SLE patients. Therefore, early detection of cardiac involvement in SLE patients is crucial for improving prognosis.

Objective To establish quality standards for stem leaf ofAstragali Radix.Methods A method of TLC identification was used for qualitative discrimination. The moisture, total ash and extracts contents of the stem leaf of Astragali Radix were determined by pharmacopoeia method. Total contents of astragaloside and astragalus polysaccharide were measured by colorimetry. The astragalosideⅣ and calycosin-7-O-β-D-glucoside contents were detected by HPLC.Results The spots of TLC were round and clear with good repeatability. The moisture contents of the stem leaf ofAstragali Radix were between 6.24%–12.24%; the total ash was between 8.21%–10.55%; the water- solubility extracts were between 12.12%–27.30%; alcohol-solubility extracts were between 6.89%–10.28%; the total contents of astragaloside were between 23.74–26.52 mg/g; astragalus polysaccharide were between 23.31–45.70 mg/g; the astragalosideⅣ contents were between 0.047%–0.18%; the calycosin-7-O-β-D-glucoside were 0.21%–0.26%. Conclusion The method is convenient, fast and repeatable, and the results are accurate and reliable, which can be used to control the quality of the stem leaf ofAstragali Radix effectively, and as the main index of the quality standard.

Objective To investigate the influence of somatostatin (SS) and protein tyrosine enzyme 1 B (PTP1B) on the proliferation and the matrix protein secretion and phosphorylation of JAK2/STAT3 of hepatic stellate cells (HSC) induced by leptin. Methods The effect of different concentrations of SS on the proliferation of activatied HSCs induced by leptin was detected with MTT assay. HSCs were divided into control group, leptin group, leptin+10-7 mol/LSS group, leptin+10-6 mol/LSS group, TIMP-1, type I collagen and PTP1B protein and mRNA. Phosphorylation of JAK2/STAT3 were detected by RT-PCR, Western bolt and ELISA assay. Results SS could promote leptin-induced proliferation of HSCs in a dose-adependent manner. SS can improve PTP1B protein and mRNA, and higher does of SS could render more increase compared with the lower does. SS could reduce TIMP-1 mRNA, type I collagen mRNA and protein expression, and make the JAK2/STAT3 dephosphorylated, and the higher SS group reduce these factors more obviously than the lower group. Conclusion SS up-regulates PTP1B expression, inhibits JAK2/STAT3 signal transduction, proliferation, and reduces TIMP-1, I collagen expression in actived HSCs induced by leptin.