Narcotic plants are strictly regulated worldwide due to their ability to extract drug alkaloids and drug precursor components. Besides the three traditional core species, cannabis, opium poppy, and coca, the misuse of psychoactive plants with addictive properties has become increasingly prevalent globally in recent years, and the establishment of accurate identification methods for such plants has become an urgent need in the field of narcotics control. Within existing identification frameworks, the conventional morphological and chemical analysis methods, despite their long-term application, have demonstrated considerable limitations. In contrast, DNA-based molecular identification techniques have achieved significant advancement in recent years due to their high specificity and stability. This review comprehensively examines current DNA-based identification approaches for narcotic plants through three key dimensions: DNA molecular marker technology, DNA barcoding technology, and emerging molecular biological techniques, and elaborates on the principles, technical characteristics, application scenarios, and research progress of each technology, providing some reference for the scientific selection of DNA identification strategies for narcotic plants in different specific scenarios.

ObjectiveTo elucidate the effects of autonomic neuromodulators [calcium chloride (CaCl₂)-acetylcholine (ACh)] on atrial electrical remodeling and histopathological changes in rats, thereby providing evidence for further investigation into the pathological mechanisms by which autonomic imbalance induces atrial fibrillation (AF). MethodsTen 8-week-old male Sprague-Dawley (SD) rats were randomly divided into experimental and control groups, with 5 rats in each group. The experimental group received daily tail vein injections of a CaCl₂-ACh mixed solution for 28 days, while the control group received an equal volume of saline. Surface electrocardiograms were recorded before and after daily administration. On day 28 of administration, under isoflurane inhalation anesthesia, echocardiography was performed, and then the rats were euthanized by exsanguination under isoflurane anesthesia for tissue collection. Body weight and heart weight of rats were measured, and electrophysiological parameters including AF inducibility, conduction velocity, and conduction dispersion in isolated rat hearts were monitored using the MappingLab multichannel electrophysiological mapping system. HE staining was performed to evaluate atrial tissue architecture and inflammatory cell infiltration. The expression levels of matrix metalloproteinase 9 (MMP-9) and interleukin-1 beta (IL-1β) were analyzed by Western blotting. Masson staining was used to quantitatively analyze the proportional distribution of collagen fibers and myocardial fibers, and to calculate the area of collagen deposition, thereby evaluating the degree of myocardial fibrosis. Wheat germ agglutinin (WGA) staining was used to evaluate morphological changes of cardiomyocytes. Dihydroethidium (DHE) staining was used to detect the level of oxidative stress in atrial myocytes. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining was used to detect atrial cell apoptosis. ResultsCompared with the control group, the experimental group showed obvious arrhythmias on electrocardiograms. Echocardiography after 28 days of administration revealed significant structural remodeling in the experimental group, with a marked increase in left atrial anteroposterior diameter (P < 0.05), and also showed cardiac dysfunction, with significant decreases in left ventricular ejection fraction and left ventricular fractional shortening (P < 0.01). Compared with the control group, the experimental group showed a significantly increased heart weight-to-body weight ratio (P < 0.05), a markedly higher AF inducibility (P < 0.001), a significantly slowed atrial conduction velocity (P < 0.05), an uneven isochronal map with irregular directions, and a significantly increased conduction dispersion (P < 0.01). HE staining showed that atrial myocytes in the experimental group were disorganized, with slight inflammatory cell infiltration. Western blotting showed that the expression levels of MMP-9 and IL-1β in the atrial tissue of the experimental group were significantly upregulated (P < 0.05). Masson staining showed a significant increase in collagen deposition and a significant increase in fibrosis area in the atrial tissue of the experimental group (P < 0.001). WGA staining showed that cardiomyocytes in the experimental group were significantly hypertrophied compared with the control group (P < 0.05). DHE staining and TUNEL staining revealed that the level of oxidative stress in atrial myocytes (P < 0.001) and the apoptotic rate (P < 0.01) were both significantly increased. Conclusion Daily tail vein injections of the autonomic neuromodulator CaCl₂-ACh mixed solution for 28 days can successfully induce AF in rats, accompanied by significant atrial structural remodeling, electrical remodeling, and oxidative stress.

Diabetic cardiomyopathy （DCM） is a common chronic complication of diabetes， categorized as consumptive thirst in traditional Chinese medicine （TCM）， and it subsequently gives rise to chest impediment. DCM is characterized by a complex pathogenesis and exhibits long-term progression with poor prognosis in clinical practice. Astragali Radix， as a medicinal material with edible value， possesses diverse active components including saponins， polysaccharides， and flavonoids. It has the effects of tonifying Qi， elevating Yang， promoting fluid production， nourishing blood， expressing toxin， and expelling pus. Modern pharmacological studies have confirmed that Astragali Radix and its active components exert therapeutic effects in various aspects such as inhibition of inflammation， alleviation of stress injury， regulation of programmed cell death， modulation of glucose and lipid metabolism， inhibition of myocardial fibrosis， and regulation of gut microbiota and metabolites， treating DCM in a multi-component， multi-target， and multi-pathway manner. The compatibility of Astragali Radix exerts both synergistic and antagonistic effects. The compound preparations and extracts of Astragali Radix are widely used in clinical practice， and the development of novel nano and gel materials and extracellular vesicles helps to improve the oral bioavailability， providing more possibilities for the clinical application of Astragali Radix in DCM， though its potential for clinical translation requires ongoing exploration. This review summarizes the TCM theoretical basis of Astragali Radix in the treatment of DCM， and integrates modern pharmacological research results to delve into the effects and mechanisms of the herb combinations， compound preparations， extracts， and new composite materials of Astragali Radix in the treatment of DCM， aiming to provide a reference for in-depth research and new drug development of Astragali Radix for DCM.

Bone remodeling is essential for maintaining skeletal integrity and mineral homeostasis and depends on the coordinated activities of osteoclasts, osteoblasts, and osteocytes. Osteoclast-mediated bone resorption must remain closely coupled with osteoblast-mediated bone formation, while osteocytes continuously sense mechanical loading and changes in the local and systemic environment. Reactive oxygen species are involved in these physiological processes, particularly in the regulation of osteoclast differentiation and osteoblast function. Once oxidative stress exceeds the capacity of cellular antioxidant systems, however, this balance may be disturbed, leading to enhanced bone resorption, impaired bone formation, and deterioration of bone quality. In recent years, ferroptosis has attracted increasing attention in studies of bone metabolism. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides, but ferroptosis-related alterations in bone tissue may occur before obvious cell death becomes detectable. Changes in the labile iron pool, membrane lipid composition, antioxidant capacity, and mitochondrial metabolism can already influence the biological behavior of bone cells at an earlier stage. On this basis, ferroptosis susceptibility may provide a useful way to describe a reversible metabolic state in which cells become increasingly vulnerable to lipid peroxidation while widespread membrane damage and terminal cell death have not yet occurred. Such a state should not be identified by a single molecular marker. A more appropriate assessment would combine changes in intracellular iron handling, lipid peroxidation, antioxidant defense, cell viability, bone-cell function, and the response to ferroptosis-related interventions. Measurements of Fe²⁺ or the labile iron pool, C11-BODIPY oxidation, 4-HNE and MDA, GPX4 activity or expression, GSH/GSSG balance, LDH release, and PI staining may therefore provide complementary information when interpreted together with functional changes and rescue experiments. Several metabolic processes may contribute to the development of ferroptosis susceptibility in the bone. Disturbances in iron uptake, ferritin storage, ferritinophagy, and ferroportin-mediated iron export can increase the availability of redox-active iron. At the same time, ACSL4- and LPCAT3-dependent incorporation of polyunsaturated fatty acids into membrane phospholipids increases the pool of oxidizable lipid substrates. Reduced activity of the system Xc^--GSH-GPX4 pathway further weakens the ability of cells to remove lipid hydroperoxides, while FSP1-CoQ and mitochondrial DHODH-CoQ systems provide additional antioxidant protection. Mitochondrial dysfunction, inflammation, and abnormalities in calcium-phosphate and endocrine regulation may further increase this metabolic pressure. Importantly, the consequences are unlikely to be identical among bone-cell populations. In osteoclasts, increased iron availability and oxidative stress may strengthen RANKL-NFATc1-associated differentiation and resorptive activity. In osteoblasts, persistent lipid peroxidation may interfere with RUNX2-related differentiation, collagen synthesis, matrix production, and mineralization before extensive cell loss occurs. Osteocytes, because of their long lifespan and specialized location within the mineralized matrix, may be particularly sensitive to chronic metabolic stress, resulting in impaired mechanosensing and disturbed RANKL- or FGF23-related feedback. Evidence linking these changes with osteoporosis, diabetes-related bone disorders, chronic kidney disease-mineral and bone disorder, inflammatory bone loss, and particle-induced osteolysis is increasing, although the strength of evidence differs among disease models. Changes in ROS, MDA, GPX4, or other individual indicators alone are insufficient to demonstrate ferroptosis-related susceptibility, and stronger conclusions require evidence of iron dependence, lipid peroxidation, temporal sequence, and reversibility. Emerging single-cell, spatial, proteomic, lipidomic, and metabolomic approaches may help identify susceptible cell populations and bone-remodeling regions more precisely, although the mineralized matrix and the effects of sample processing remain important technical limitations. Overall, ferroptosis susceptibility may represent an intermediate metabolic state linking disturbances in iron and redox homeostasis with progressive uncoupling of bone resorption and formation. Clarifying its cell-specific features, temporal development, and reversible window may improve our understanding of how chronic metabolic stress contributes to bone remodeling disorders and may also provide a basis for earlier and more targeted intervention.

Objective To explore enteral nutrition support and analyze its influencing factors in elderly patients with ischemic stroke. Methods A total of 328 patients with ischemic stroke in General Hospital of Western Theater Command were enrolled for nutritional screening between July 2020 and February 2024. Corresponding nutritional support plans were selected to investigate the compliance of patients with enteral nutrition support. Patients were divided into a standard group (n=140) and a non-standard group (n=97) based on whether their calorie intake met the standard. The effects of different clinical characteristics on enteral nutrition support were explored, and logistic analysis was used to analyze the influencing factors of non-standard enteral nutrition support. Results In the 328 patients with ischemic stroke, proportions of total parenteral nutrition support, total enteral nutrition support, and parenteral/enteral nutrition support were 25.30%, 27.74% and 46.95%, respectively. The proportions of vomiting or regurgitation, gastric residual volume >100 mL, mechanical ventilation and use of antibiotics >2 in the non-standard group were higher than those in the standard group (P<0.05). Logistic analysis showed that the above clinical characteristics were risk factors influencing patients with enteral nutrition support and parenteral/enteral nutrition support. Conclusion Vomiting or regurgitation , gastric residual volume, mechanical ventilation, and amount of antibiotics used are important influencing factors of enteral nutrition support in patients. Clinicians should pay attention to the above clinical characteristics.

ObjectiveTo explore the mechanism by which Ruyan Neixiao cream （RUC） induces ferroptosis in breast precancerous lesion （BPL） cells， and to enrich the theoretical foundation for its use in the treatment of BPL. MethodsThe inhibition of cell proliferation by 1%， 2%， and 4% concentrations of Ruyanneixiao Cream transdermal solution （RUT） was assessed using cell counting kit-8 （CCK-8） and a colony formation assay. Reactive oxygen species （ROS） were measured using the DCFH-DA probe， and the levels of ferrous ions （Fe²⁺）， glutathione （GSH）， and malondialdehyde （MDA） were determined using appropriate kits. Lipid peroxidation was detected with the C11-BODIPY^581/591 fluorescent probe. The expression of nuclear factor E₂-related factor 2 （Nrf2）， solute carrier family 7 member 11 （SLC7A11）， and glutathione peroxidase 4 （GPX4） proteins was analyzed by Western blot. The BPL rat model was constructed using 2，2′-bis（hydroxymethyl）butyric acid （DMBA） combined with estrogen and progesterone， and the rats were treated with RUC for external application. After the 12^th cycle， the rats were euthanized， and histopathological changes in breast tissue were observed by hematoxylin-eosin （HE） staining. Fe²⁺ and MDA levels in breast tissue were measured using corresponding kits. The expression of Nrf2， SLC7A11， and GPX4 proteins in BPL rat breast tissue was detected by immunohistochemistry （IHC） and Western blot. ResultsCompared with the matrix group， the cell viability of MCF-10AT cells in the 1%， 2%， and 4% RUT groups was significantly reduced （P<0.05） in a concentration-dependent manner， with the 24-hour half inhibitory concentration （IC₅₀） being 2.23%. Compared with the 4% RUT group， cell viability in the RUT + Fer-1 group was significantly increased （P<0.05）. Compared with the matrix group， the colony formation rates of MCF-10AT cells in the 1%， 2%， and 4% RUT groups were significantly decreased （P<0.05）. Compared with the 4% RUT group， the cell colony formation rate of the RUT + Fer-1 group was significantly increased （P<0.05）. Compared with the matrix group， the levels of ROS and Fe²⁺ in the 1%， 2%， and 4% RUT groups were significantly increased （P<0.05）， while GSH levels were significantly decreased （P<0.05）， and MDA and lipid peroxidation levels were significantly increased （P<0.05）. Compared with the 4% RUT group， ROS and Fe²⁺ levels in the RUT + Fer-1 group were significantly reduced （P<0.05）， while GSH levels were significantly increased （P<0.05）， and MDA and lipid peroxidation levels were significantly reduced （P<0.05）. Compared with the matrix group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the 1%， 2%， and 4% RUT groups were significantly decreased （P<0.05）. Compared with the 4% RUT group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the RUT + Fer-1 group were significantly increased （P<0.05）. In the in vivo experiment， compared with the matrix group， the breast tissue histopathological status of the BPL rats in the RUC group was effectively improved， with less dilatation of the mammary ducts and more orderly duct arrangement. No pathological morphology indicative of invasive cancer was observed. Compared with the matrix group， Fe²⁺ and MDA levels in the mammary tissue of the RUC group were significantly increased （P<0.05）. Compared with the matrix group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the mammary tissue of the RUC group were significantly reduced （P<0.05）. ConclusionRUC may induce ferroptosis in BPL cells by inhibiting the Nrf2/SLC7A11/GPX4 signaling pathway， increasing Fe²⁺ accumulation， and promoting lipid peroxidation.

ObjectiveTo explore the mechanism by which Ruyan Neixiao cream （RUC） induces ferroptosis in breast precancerous lesion （BPL） cells， and to enrich the theoretical foundation for its use in the treatment of BPL. MethodsThe inhibition of cell proliferation by 1%， 2%， and 4% concentrations of Ruyanneixiao Cream transdermal solution （RUT） was assessed using cell counting kit-8 （CCK-8） and a colony formation assay. Reactive oxygen species （ROS） were measured using the DCFH-DA probe， and the levels of ferrous ions （Fe²⁺）， glutathione （GSH）， and malondialdehyde （MDA） were determined using appropriate kits. Lipid peroxidation was detected with the C11-BODIPY^581/591 fluorescent probe. The expression of nuclear factor E₂-related factor 2 （Nrf2）， solute carrier family 7 member 11 （SLC7A11）， and glutathione peroxidase 4 （GPX4） proteins was analyzed by Western blot. The BPL rat model was constructed using 2，2′-bis（hydroxymethyl）butyric acid （DMBA） combined with estrogen and progesterone， and the rats were treated with RUC for external application. After the 12^th cycle， the rats were euthanized， and histopathological changes in breast tissue were observed by hematoxylin-eosin （HE） staining. Fe²⁺ and MDA levels in breast tissue were measured using corresponding kits. The expression of Nrf2， SLC7A11， and GPX4 proteins in BPL rat breast tissue was detected by immunohistochemistry （IHC） and Western blot. ResultsCompared with the matrix group， the cell viability of MCF-10AT cells in the 1%， 2%， and 4% RUT groups was significantly reduced （P<0.05） in a concentration-dependent manner， with the 24-hour half inhibitory concentration （IC₅₀） being 2.23%. Compared with the 4% RUT group， cell viability in the RUT + Fer-1 group was significantly increased （P<0.05）. Compared with the matrix group， the colony formation rates of MCF-10AT cells in the 1%， 2%， and 4% RUT groups were significantly decreased （P<0.05）. Compared with the 4% RUT group， the cell colony formation rate of the RUT + Fer-1 group was significantly increased （P<0.05）. Compared with the matrix group， the levels of ROS and Fe²⁺ in the 1%， 2%， and 4% RUT groups were significantly increased （P<0.05）， while GSH levels were significantly decreased （P<0.05）， and MDA and lipid peroxidation levels were significantly increased （P<0.05）. Compared with the 4% RUT group， ROS and Fe²⁺ levels in the RUT + Fer-1 group were significantly reduced （P<0.05）， while GSH levels were significantly increased （P<0.05）， and MDA and lipid peroxidation levels were significantly reduced （P<0.05）. Compared with the matrix group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the 1%， 2%， and 4% RUT groups were significantly decreased （P<0.05）. Compared with the 4% RUT group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the RUT + Fer-1 group were significantly increased （P<0.05）. In the in vivo experiment， compared with the matrix group， the breast tissue histopathological status of the BPL rats in the RUC group was effectively improved， with less dilatation of the mammary ducts and more orderly duct arrangement. No pathological morphology indicative of invasive cancer was observed. Compared with the matrix group， Fe²⁺ and MDA levels in the mammary tissue of the RUC group were significantly increased （P<0.05）. Compared with the matrix group， the protein expression levels of Nrf2， SLC7A11， and GPX4 in the mammary tissue of the RUC group were significantly reduced （P<0.05）. ConclusionRUC may induce ferroptosis in BPL cells by inhibiting the Nrf2/SLC7A11/GPX4 signaling pathway， increasing Fe²⁺ accumulation， and promoting lipid peroxidation.

Objective: To systematically analyze the revisions content and technological development trends of microbiological standards in the Chinese Pharmacopoeia (ChP) 2025 Edition, and explore its novel requirements in risk-based pharmaceutical product lifecycle management.
Methods: A comprehensive review was conducted on 26 microbiological-related standards to summarize the revision directions and scientific implications from perspectives including the revision overview, international harmonization of microbiological standards, risk-based quality management system, and novel tools and methods with Chinese characteristics.
Results: The ChP 2025 edition demonstrates three prominent features in microbiological-related standards: enhanced international harmonization, introduced emerging molecular biological technologies, and established a risk-based microbiological quality control system.
Conclusion: The new edition of the Pharmacopoeia has systematically constructed a microbiological standard system, which significantly improves the scientificity, standardization and applicability of the standards, providing a crucial support for advancing the microbiological quality control in pharmaceutical industries of China.

ObjectiveTo investigate the association of serum exosomal microRNAs （miRNAs） with hepatic inflammatory injury and histological outcomes in patients with chronic hepatitis B （CHB）. MethodsPeripheral serum samples were collected from six healthy adults and six patients with CHB， and size exclusion chromatography was used to extract exosomes. Small RNA sequencing and transcriptomic analysis were used to identify the serum exosomal miRNAs associated with liver inflammatory injury and fibrosis， and quantitative real-time PCR was used for validation in a mouse model of acute liver injury induced by lipopolysaccharide/D-galactosamine， a rat model of liver fibrosis induced by carbon tetrachloride， and 84 CHB patients undergoing liver biopsy twice before and after treatment. The independent-samples t test was used for comparison of normally distributed continuous data between two groups； an analysis of variance was used for comparison between multiple groups， and the Tukey test was used for further comparison between two groups. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups； the Kruskal-Wallis H test was used for comparison between multiple groups， and the Dunn test was used for further comparison between two groups. The chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. The univariate and multivariate Logistic regression analyses were used to investigate influencing factors. ResultsAbnormal expression of serum exosomal miR-122-5p was observed in patients with CHB， and it was downregulated in patients with confluent necrosis and advanced fibrosis. In the mouse model of acute liver injury and the rat model of liver fibrosis， compared with the control group， the model group had a significant reduction in the expression level of miR-122-5p in the liver （P=0.048 and 0.014）， and compared with the patients with mild liver injury， the patients with severe confluent necrosis and advanced fibrosis showed a significant reduction in the expression level of miR-122-5p in liver tissue （P<0.05）. Among the 84 CHB patients， the patients with severe hepatic confluent necrosis or advanced liver fibrosis had a significantly lower expression level of serum exosomal miR-122-5p than those with mild liver injury （P<0.001 and P=0.003）. The multivariate Logistic regression analysis showed that the expression level of miR-122-5p was an independent influencing factor for confluent necrosis （odds ratio ［OR］=0.001， 95% confidence interval ［CI］： 0.000‍ ‍—‍ ‍0.037， P=0.005） and liver fibrosis degree （OR=0.568， 95%CI： 0.331‍ ‍—‍ ‍0.856， P=0.019）. In addition， compared with the patients with low expression of miR-122-5p， the patients with high expression of miR-122-5p before treatment had a significantly higher reversal rate of liver fibrosis after 72 weeks of antiviral therapy （64.3% vs 38.1%， P=0.029）. ConclusionSerum exosomal miR-122-5p in CHB patients is closely associated with the progression of hepatic confluent necrosis and fibrosis， and the reduction in the expression level of miR-122-5p may aggravate hepatic confluent necrosis， promote the progression of fibrosis， and affect the histological outcome of CHB patients after antiviral therapy.

OBJECTIVE To explore the main factors influencing the blood concentration of duloxetine， and provide a scientific basis for the individualized use of duloxetine. METHODS Retrospective analysis was conducted on 434 inpatients with depressive disorders at the First Hospital of Hebei Medical University， who were treated with duloxetine and underwent blood concentration monitoring between January 2022 and April 2024. The study examined the impact of various factors， including gender， age， body mass index （BMI）， gene phenotypes， combined medication， drug type （original/generic）， and genotyping results of gene single nucleotide polymorphism loci， on blood concentration and the concentration-to-dose （C/D） after dose adjustment. RESULTS The blood concentration of duloxetine was 76.65 （45.57， 130.31） ng/mL， and C/D was 0.96 （0.63， 1.60） ng·d/（mL·mg）. The blood concentration of duloxetine was positively correlated with the daily dose of administration （R2＝0.253 7， P＜0.001）. Blood concentration of duloxetine in 38.94% of patients exceeded the recommended range specified in the guidelines. Gender， age， BMI， combined use of CYP2D6 enzyme inhibitors， and CYP2D6 and CYP1A2 phenotypes had significant effects on C/D of duloxetine （P＜0.05）. CONCLUSIONS The patient’s age， gender， BMI， combined medication， and genetic phenotypes are closely related to the blood concentration of duloxetine.