OBJECTIVE To ensure the safety of patients’ drug use and control the risk of medical insurance expenditure by upgrading the pre-prescription review system to conduct pre-review on prescriptions from internet hospitals and external prescriptions， as well as to review the payment methods of drugs （including in-hospital and external drug dispensing）. METHODS The data interfaces of prescriptions from internet hospitals and external prescriptions were integrated to achieve real-time rational drug use intervention. Additionally， an intelligent review project for payment method was added to precisely intervene in the medical insurance payment methods of drugs. The effect of the system upgrade was evaluated by comparing the qualification rates of prescriptions from internet hospitals and external prescriptions and the suspected amounts of drug violations from January to April 2025 （before the system upgrade） and May to August 2025 （after the system upgrade）. RESULTS After the upgrade of the pre-prescription review system， the qualification rates of prescriptions from internet hospitals and external prescriptions increased by 3.5% [95% confidence interval （CI）＝0.3%-6.7%， P ＝0.037 ] ； the suspected amounts of drug violations decreased to 52.9% of the pre-upgrade level （95%CI＝31.6%-88.5%， P ＝0.026）， and the average monthly sequential decrease was 29.5% （95%CI＝12.2%-43.4%， P ＝0.012）. Moreover， the addition of the intelligent review project for payment methods promoted the management of off-label drug use in our hospital. After the upgrade， a total of 79 filling valid applications for off-label drug use were received and archived. CONCLUSIONS The upgrade of the pre-prescription review system effectively improves the review qualification rates of prescriptions from internet hospitals and external prescriptions and the accuracy of medical insurance payment for drugs， and strengthens the supervision of off-label drug use， achieving dual guarantees of clinical rationality and medical insurance compliance.

Both type 2 diabetes mellitus (T2DM) and metabolic associated fatty liver disease (MAFLD) fall within the spectrum of metabolic diseases, and they exhibit a bi-directional causal relationship and robust reciprocal association. Their shared pathological cornerstone is insulin resistance (IR), which involves the interplay of mitochondrial dysfunction and chronic inflammation, forming a cascading pathological process of “IR-mitochondrial dysfunction-inflammation”. This largely explains the notable upward trend in T2DM-MAFLD co-occurrence observed over recent years. Exercise intervention, as a safe and effective non-pharmacological approach, can improve the pathological progression of these patients at multiple levels. Following the logical framework of “pathogenesis-efficacy comparison-molecular mechanisms-clinical translation”, this article systematically compares the efficacy and molecular mechanisms of moderate-intensity continuous training (MICT), resistance exercise, high-intensity interval training (HIIT), and combined training. MICT reduces intrahepatic triglycerides by promoting lipolysis and improving cardiorespiratory fitness; resistance exercise increases muscle mass and basal metabolic rate, offering unique advantages in preserving muscle while reducing fat and improving insulin sensitivity; HIIT is a time-efficient exercise modality that enhances patients’ cardiorespiratory fitness and insulin sensitivity by alternating brief periods of vigorous exertion with recovery periods, with a prominent short-term triglyceride-lowering effect; combined training produces synergistic effects, comprehensively improving glucolipid metabolism and showing the best long-term adherence. Mechanistically, exercise exerts its beneficial effects through three common pathways: (1) AMPK-mediated lipid oxidation and mitochondrial biogenesis; (2) IRS/PI3K/Akt-mediated insulin signaling sensitization; and (3) Nrf2/ARE anti-oxidation and TGF-β/Smads anti-fibrosis regulation. Different exercise modalities activate these pathways with distinct emphases: MICT most directly and persistently activates the AMPK pathway; resistance exercise uniquely improves IRS/PI3K/Akt signaling through muscle mass gain; HIIT induces the highest AMPK activation intensity and triggers unique lactate-mediated signaling regulation; combined training integrates the above multiple mechanistic advantages. For clinical translation, multidisciplinary team collaboration is essential to ensure safety and adherence. Individualized prescriptions should be formulated according to the FITT-VP principle and patient phenotypes—frequency of 3-5 sessions/week of aerobic exercise combined with 2-3 sessions/week of resistance exercise; intensity of moderate-intensity (40%-60% heart rate reserve (HRR))aerobic exercise and 60%-80% of one-repetition maximum (1-RM) for resistance exercise; time of at least 150 min/week of moderate-intensity aerobic exercise, 30-60 min per session; type of combined training as the preferred modality; total volume of≥500-1 000 MET-min/week; and progression adjusted every 4-6 weeks—with real-time adjustments supported by wearable devices, ultimately forming a closed-loop management system from initial assessment to long-term follow-up. Notably, current studies have limitations such as small sample sizes and short intervention periods. Future research should focus on long-term follow-up, multi-omics biomarkers, and combined exercise-drug strategies. In conclusion, the systematic integration of structured, individualized, and sustainable exercise interventions into the multidisciplinary management pathway for patients with T2DM complicated by MAFLD is an urgent need in current clinical practice.

Bone metastases are a common and serious complication of solid tumors such as breast cancer, prostate cancer, lung cancer, and kidney cancer, and occur at a high rate in patients with advanced cancer. This pathological process not only frequently leads to skeletal-related events such as severe bone pain, pathological fractures, spinal cord compression, and hypercalcemia—conditions that severely impact patients’ quality of life—but may also significantly increase the risk of death. Cancer bone metastasis is a complex, multistage cascade involving key steps such as the detachment of tumor cells from the primary tumor, their invasion and entry into the bloodstream, and their colonization, dormancy, and reactivation within the bone microenvironment. In recent years, exercise—as a safe and easily implementable non-pharmacological intervention—has demonstrated significant potential in inhibiting bone metastasis, improving the bone microenvironment, and alleviating related clinical symptoms. Its mechanisms of action may involve multiple levels. First, at the mechanical load level, mechanical signals generated by exercise can directly act on bone cells, inhibiting tumor cell infiltration and colonization by regulating endothelial cell permeability and osteoclast activity. Second, at the endocrine and paracrine levels, exercise can alter the expression profiles of microRNAs (such as miR-486 and miR-34b) carried by extracellular vesicles and particles (EVPs) in the circulation, thereby inhibiting tumor cell proliferation and migration by targeting cell cycle-related genes. Furthermore, exercise can remodel the immune microenvironment, enhance the cytotoxic activity of antitumor immune cells, and improve oxygen supply to tumor tissues, thereby alleviating hypoxia-induced immunosuppression. Finally, at the metabolic intervention level, exercise can induce systemic metabolic reprogramming, increasing the nutritional demands of normal tissues, thereby competing with tumor cells for nutrients and forming a “metabolic barrier” in distal organs such as bones. This article reviews the pathogenesis and classification of bone metastases, including osteolytic, osteogenic, and mixed types, and elaborates in detail on the complex processes by which tumor cells undergo colonization, dormancy, and reactivation within the bone microenvironment. Furthermore, based on a comprehensive analysis of human and animal studies on exercise interventions for bone metastases, this paper highlights the mechanisms by which exercise inhibits tumor formation, growth, and spread through the regulation of mechanical loading, extracellular vesicles and granules, as well as via immune and metabolic pathways, thereby interfering with bone metastasis. However, the array of exercise modalities and intensities available for patients grappling with the challenges of cancer-related bone metastases remains markedly constrained, and the formulation of tailored exercise prescriptions continues to be devoid of robust, evidence-based medical backing. This review aims to explore the effects of exercise on bone health in patients with bone metastases, analyze the factors and considerations that should be taken into account in exercise prescriptions, and provide new theoretical support and insights for developing personalized exercise programs for these patients and further advancing relevant clinical research. Future research directions should include the development of evidence-based, personalized exercise prescriptions and further clarification of the safety boundaries and best practice standards for exercise interventions, thereby promoting the advancement of relevant clinical research and ultimately improving patients’ clinical outcomes and quality of life.

Isoliquiritigenin (ISL) is a chalcone compound isolated from licorice, known for its anti-diabetic, anti-cancer, and antioxidant properties. Our previous study has demonstrated that ISL effectively lowers blood glucose levels in type 2 diabetes mellitus (T2DM) mice and improves disturbances in glucolipid and energy metabolism induced by T2DM. This study aims to further investigate the effects of ISL on alleviating abnormal endoplasmic reticulum stress (ERS) caused by T2DM and to elucidate its molecular mechanisms. In vivo experiments were conducted using 8-week-old SPF male C57BL/6J mice. The T2DM animal model was established by high-fat and high-sugar diet combined with intraperitoneal injections of streptozotocin (STZ), in compliance with the ethical guidelines set by the Animal Welfare Committee of Beijing University of Chinese Medicine (approval number: BUCM-2022021503-1134). In vitro experiments employed human liver cancer HepG2 cells, which were induced with tunicamycin (TM) to establish the ERS cell model. Transcriptomic sequencing was used to analyze changes in gene expression in the liver samples of T2DM mice following ISL treatment. Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to assess the regulatory effects of ISL on key ERS genes. Enzyme-linked immunosorbent assay (ELISA), Western blot (WB), and immunofluorescence techniques were used to evaluate ISL's effects on ERS-related proteins. Results indicate that ISL significantly downregulates the expression of ERS-related genes, reduces the level of glucose-regulated protein 78 (GRP78), and inhibits the phosphorylation of protein kinase RNA-like endoplasmic reticulum kinase (PERK), thereby alleviating abnormal ERS induced by T2DM. Additionally, ISL increases the protein levels of insulin receptor substrate (IRS) 1 and IRS2 and enhances the phosphorylation of protein kinase B (Akt), thereby improving insulin sensitivity. In conclusion, ISL is able to alleviate T2DM associated symptoms by improving abnormal ERS and enhancing insulin sensitivity.

ObjectiveTo investigate the effects of different concentrations of Shaoyaotang-containing serum on lipopolysaccharide （LPS）-induced inflammation of human colorectal adenocarcinoma （Caco-2） cells by inhibiting apoptosis via activating the tumor necrosis factor （TNF） receptor superfamily member 6 （Fas）/Fas ligand （FasL） pathway. MethodsCaco-2 cells were allocated into blank， model （LPS， 10 mg·L^-1）， Shaoyaotang-containing serum （5%， 10%， 15%， 20%）， and Fas inhibitor （KR-33493， 20 mmol·L^-1） groups. Except the blank group， the other groups were stimulated with 10 mg·L^-1 LPS for 24 h for the modeling of inflammation. After successful modeling， the blank， Fas inhibitor， and model groups were treated with blank serum， and the Shaoyaotang-containing serum groups were treated with the serum samples at corresponding concentrations for 24 h. The Fas inhibitor group was subjected to KR-33493 pretreatment for 1 h. Cell proliferation and viability were examined by the cell-counting kit-8 （CCK-8） method. The levels of interleukin （IL）-6， IL-1β， and TNF-α were measured by enzyme-linked immunosorbent assay. Apoptosis was detected by flow cytometry. The protein and mRNA levels of Fas， FasL， cysteinyl aspartate-specific proteinase （Caspase）-3， Caspase-9， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsCompared with the blank group， the model group presented a decrease in cell survival rate （P<0.01）. Compared with that in the model group， the cell survival rate showed no significant change in the 5% Shaoyaotang-containing serum group but increased in the 10%， 15%， and 20% Shaoyaotang-containing serum groups （P<0.01）. Since there was no statistical difference between the 5% Shaoyaotang-containing serum group and the model group， 10%， 15%， and 20% Shaoyaotang-containing sera were selected for the follow-up study. Compared with the blank group， the model group showed risen levels of IL-6， IL-1β， and TNF-α （P<0.01）， an increased apoptosis rate （P<0.01）， up-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.01）， and down-regulated protein and mRNA levels of Bcl-2 （P<0.01）. Compared with the model group， the Fas inhibitor group and the 10%， 15%， and 20% Shaoyaotang-containing serum groups showed declined levels of IL-6， IL-1β， and TNF-α （P<0.01）， decreased apoptosis rates （P<0.01）， down-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of Bcl-2 （P<0.05， P<0.01）. In addition， the 15% and 20% Shaoyaotang-containing serum groups had lower levels of IL-6， IL-1β， and TNF-α （P<0.05， P<0.01）， lower apoptosis rates （P<0.05， P<0.01）， lower protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and higher protein and mRNA levels of Bcl-2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can reduce the content of inflammatory factors in Caco-2 cells， down-regulate the protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax， and up-regulate the protein and mRNA levels of Bcl-2 under the intervention of LPS by regulating the Fas/FasL pathway and inhibiting the apoptosis of intestinal epithelial cells in ulcerative colitis.

ObjectiveTo investigate the protective effect and mechanism of Shaoyaotang （SYD） on the lipopolysaccharide （LPS）-induced damage of tight junction proteins in the human colorectal adenocarcinoma （Caco-2） cell model of inflammation via the Ras homolog gene family member A （RhoA）/Rho-associated coiled-coil forming protein kinase （ROCK） pathway. MethodsCaco-2 cells were grouped as follows： Blank， model （LPS， 10 mg·L^-1）， SYD-containing serum （10%， 15%， and 20%）， and inhibitor （Fasudil， 25 μmol·L^-1）. After 24 hours of intervention， the cell viability in each group was examined by the cell-counting kit 8 （CCK-8） method. Enzyme-linked immunosorbent assay was employed to determine the levels of endothelin-1 （ET-1）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of RhoA， ROCK2， claudin-5， and zonula occludens-1 （ZO-1） in cells of each group. ResultsCompared with the blank group， the model group showcased a marked reduction in the cell viability （P<0.01）， elevations in the levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， declines in both mRNA and protein levels of ZO-1 and claudin-5 （P<0.01）， and rises in mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Compared with the model group， the Shaoyaotang-containing serum （10%， 15%， and 20%） groups had enhanced cell viability （P<0.01）， lowered levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， up-regulated mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and down-regulated mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Moreover， the inhibitor group and the 15% and 20% Shaoyaotang-containing serum groups had lower levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， higher mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and lower mRNA and protein levels of RhoA and ROCK2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can lower the levels of LPS-induced increases in levels of inflammatory cytokines and endothelin to ameliorate the damage of tight junction proteins of the Caco-2 cell model of inflammation by regulating the expression of proteins in the RhoA/ROCK pathway.

ObjectiveTo investigate the effects of different concentrations of Shaoyaotang-containing serum on lipopolysaccharide （LPS）-induced inflammation of human colorectal adenocarcinoma （Caco-2） cells by inhibiting apoptosis via activating the tumor necrosis factor （TNF） receptor superfamily member 6 （Fas）/Fas ligand （FasL） pathway. MethodsCaco-2 cells were allocated into blank， model （LPS， 10 mg·L^-1）， Shaoyaotang-containing serum （5%， 10%， 15%， 20%）， and Fas inhibitor （KR-33493， 20 mmol·L^-1） groups. Except the blank group， the other groups were stimulated with 10 mg·L^-1 LPS for 24 h for the modeling of inflammation. After successful modeling， the blank， Fas inhibitor， and model groups were treated with blank serum， and the Shaoyaotang-containing serum groups were treated with the serum samples at corresponding concentrations for 24 h. The Fas inhibitor group was subjected to KR-33493 pretreatment for 1 h. Cell proliferation and viability were examined by the cell-counting kit-8 （CCK-8） method. The levels of interleukin （IL）-6， IL-1β， and TNF-α were measured by enzyme-linked immunosorbent assay. Apoptosis was detected by flow cytometry. The protein and mRNA levels of Fas， FasL， cysteinyl aspartate-specific proteinase （Caspase）-3， Caspase-9， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsCompared with the blank group， the model group presented a decrease in cell survival rate （P<0.01）. Compared with that in the model group， the cell survival rate showed no significant change in the 5% Shaoyaotang-containing serum group but increased in the 10%， 15%， and 20% Shaoyaotang-containing serum groups （P<0.01）. Since there was no statistical difference between the 5% Shaoyaotang-containing serum group and the model group， 10%， 15%， and 20% Shaoyaotang-containing sera were selected for the follow-up study. Compared with the blank group， the model group showed risen levels of IL-6， IL-1β， and TNF-α （P<0.01）， an increased apoptosis rate （P<0.01）， up-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.01）， and down-regulated protein and mRNA levels of Bcl-2 （P<0.01）. Compared with the model group， the Fas inhibitor group and the 10%， 15%， and 20% Shaoyaotang-containing serum groups showed declined levels of IL-6， IL-1β， and TNF-α （P<0.01）， decreased apoptosis rates （P<0.01）， down-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of Bcl-2 （P<0.05， P<0.01）. In addition， the 15% and 20% Shaoyaotang-containing serum groups had lower levels of IL-6， IL-1β， and TNF-α （P<0.05， P<0.01）， lower apoptosis rates （P<0.05， P<0.01）， lower protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and higher protein and mRNA levels of Bcl-2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can reduce the content of inflammatory factors in Caco-2 cells， down-regulate the protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax， and up-regulate the protein and mRNA levels of Bcl-2 under the intervention of LPS by regulating the Fas/FasL pathway and inhibiting the apoptosis of intestinal epithelial cells in ulcerative colitis.

ObjectiveTo investigate the protective effect and mechanism of Shaoyaotang （SYD） on the lipopolysaccharide （LPS）-induced damage of tight junction proteins in the human colorectal adenocarcinoma （Caco-2） cell model of inflammation via the Ras homolog gene family member A （RhoA）/Rho-associated coiled-coil forming protein kinase （ROCK） pathway. MethodsCaco-2 cells were grouped as follows： Blank， model （LPS， 10 mg·L^-1）， SYD-containing serum （10%， 15%， and 20%）， and inhibitor （Fasudil， 25 μmol·L^-1）. After 24 hours of intervention， the cell viability in each group was examined by the cell-counting kit 8 （CCK-8） method. Enzyme-linked immunosorbent assay was employed to determine the levels of endothelin-1 （ET-1）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of RhoA， ROCK2， claudin-5， and zonula occludens-1 （ZO-1） in cells of each group. ResultsCompared with the blank group， the model group showcased a marked reduction in the cell viability （P<0.01）， elevations in the levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， declines in both mRNA and protein levels of ZO-1 and claudin-5 （P<0.01）， and rises in mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Compared with the model group， the Shaoyaotang-containing serum （10%， 15%， and 20%） groups had enhanced cell viability （P<0.01）， lowered levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， up-regulated mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and down-regulated mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Moreover， the inhibitor group and the 15% and 20% Shaoyaotang-containing serum groups had lower levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， higher mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and lower mRNA and protein levels of RhoA and ROCK2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can lower the levels of LPS-induced increases in levels of inflammatory cytokines and endothelin to ameliorate the damage of tight junction proteins of the Caco-2 cell model of inflammation by regulating the expression of proteins in the RhoA/ROCK pathway.

The circadian clock plays a critical role in regulating various physiological processes, including gene expression, metabolic regulation, immune response, and the sleep-wake cycle in living organisms. Post-translational modifications (PTMs) are crucial regulatory mechanisms to maintain the precise oscillation of the circadian clock. By modulating the stability, activity, cell localization and protein-protein interactions of core clock proteins, PTMs enable these proteins to respond dynamically to environmental and intracellular changes, thereby sustaining the periodic oscillations of the circadian clock. Different types of PTMs exert their effects through distincting molecular mechanisms, collectively ensuring the proper function of the circadian system. This review systematically summarized several major types of PTMs, including phosphorylation, acetylation, ubiquitination, SUMOylation and oxidative modification, and overviewed their roles in regulating the core clock proteins and the associated pathways, with the goals of providing a theoretical foundation for the deeper understanding of clock mechanisms and the treatment of diseases associated with circadian disruption.
Protein Processing, Post-Translational/physiology* ; Circadian Rhythm/physiology* ; Humans ; Animals ; CLOCK Proteins/physiology* ; Circadian Clocks/physiology* ; Phosphorylation ; Acetylation ; Ubiquitination ; Sumoylation

The phase changes and quantity-quality transfer of 17 batches of Ostreae Concha(Ostrea rivularis) during the raw material-calcined decoction pieces-standard decoction process were analyzed. The content of calcium carbonate(CaCO_3), the main component, was determined by chemical titration, and the extract yield and transfer rate were calculated. The CaCO_3 content in the raw material, calcined decoction pieces, and standard decoction was 94.39%-98.80%, 95.03%-99.22%, and 84.58%-90.47%, respectively. The process of raw material to calcined decoction pieces showed the yield range of 96.85% to 98.55% and the CaCO_3 transfer rate range of 96.92% to 99.27%. The process of calcined decoction pieces to standard decoction showed the extract yield range of 2.86% to 5.48% and the CaCO_3 transfer rate range of 2.59% to 5.13%. The results of X-ray fluorescence(XRF) assay showed that the raw material, calcined decoction pieces, and standard decoction mainly contained Ca, Na, Mg, Si, Br, Cl, Al, Fe, Cr, Mn, and K. The chemometric results showed an increase in the relative content of Cr, Fe, and Si from raw material to calcined decoction pieces and an increase in the relative content of Mg, Al, Br, K, Cl, and Na from calcined decoction pieces to standard decoction. X-ray diffraction(XRD) was employed to establish XRD characteristic patterns of the raw material, calcined decoction pieces, and standard decoction. The XRD results showed that the main phase of all three was calcite, and no transformation of crystalline form or generation of new phase was observed. Fourier transform infrared spectroscopy(FTIR) was employed to establish the FTIR characteristic spectra of the raw material, calcined decoction pieces, and standard decoction. The FTIR results showed that the raw material had internal vibrations of O-H, C-H, C=O, C-O, and CO■ groups. Due to the loss of organic matter components after calcination, no information about the vibrations of C-H, C=O, and C-O groups was observed in the spectra of calcined decoction pieces and standard decoction. In summary, this study elucidated the quantity-quality transfer and phase changes in the raw material-calcined decoction pieces-standard decoction process by determining the CaCO_3 content, calculating the extract yield and transfer rate, and comparing the element changes, FTIR characteristic spectra, and XRD characteristic pattern. The results were reasonable and reliable, laying a foundation for the subsequent process research and quality control of the formula granules of calcined Ostreae Concha(O. rivularis Gould), and providing ideas and methods for the quality control of the whole process of raw material-decoction pieces-standard decoction-formula granules of Ostreae Concha and other testacean traditional Chinese medicine.
Drugs, Chinese Herbal/isolation & purification* ; Calcium Carbonate/analysis* ; Quality Control