To investigate the mechanism of Shanzha（Hawthorn）extract affecting T cell differentiation and regulating blood lipid level in dyslipidemic mice through neutrophil extracellular trap（NETs）.

Fifty male 6-week-old C57BL/6 J mice were acclimatized for 1 week, 10 mice were fed with normal chow and 40 mice were fed with 60% high-fat chow to establish a high-fat mouse model. 4 weeks after modeling, the high-fat mice were randomly divided into a high-fat diet（HFD）group, a HFD + Shanzha（Hawthorn）extract group, and a HFD + NETs inhibitor carrier solvent group, HFD + NETs inhibitor GSK484 group. The mice in the HFD + Hawthorn extract group were treated with Shanzha（Hawthorn）extract by gavage［5.2 g/（kg·d）］. The mice in the HFD + NETs inhibitor GSK484 group were intraperitoneally injected with GSK484［4 mg/（kg·d）］. The mice in the HFD + NETs inhibitor carrier solvent group were intraperitoneally injected with an equal amount of carrier solvent, and the mice in the control group and the HFD group were injected with an equal amount of distilled water at the same time. The equal amount of the distilled water was administered orally. After 4 weeks of drug administration, the levels of serum total cholesterol, triglyceride, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were measured by biochemical analyzer. The levels of serum interferon-γ（IFN-γ）, interleukin-4（IL-4）, interleukin-10（IL-10）, interleukin-17A（IL-17A）and interleukin-21（IL-21）were measured by enzyme-linked immunosorbent assay（ELISA）. The immunofluorescence double staining was used for the expressions of neutrophil myeloperoxidase（MPO）and citrullinated histone（CitH3）to analyze the formation of NETs, and Western blotting was used for the protein expressions of peripheral blood mononuclear cell T-box transcription factor 21（TBx21）, Gata-binding protein 3（Gata-3）, retinoic acid-related orphan nuclear receptor γt（RORγt）, forkhead-like transcription factor 3（Foxp3）and B-cell lymphoma 6（Bcl-6）.

Compared with those in the normal control group, the high-fat diet mice showed significant increase in body weights, significant increase in the levels of TC, TG and LDL-C, significant decrease in HDL-C levels, significant increase in the levels of IFN-γ, IL-17A and IL-21, and significant decrease in the levels of IL-4 and IL-10, significant increase in the expression levels of MPO and CitH3, and significant increase in the expression levels of protein expressions of Tbx21 and RORγt in the peripheral blood, and significant decrease in the levels of Gata3, Foxp3 and Bcl-6. Compared with those in the HDF group, the mice in the HFD + Shanzha（Hawthorn）extract group and the HFD + NETs inhibitor GSK484 group had significantly lower body weights, significantly lower levels of TC, TG and LDL-C, significantly higher levels of HDL-C, significantly lower levels of IFN-γ, whereas IL-10 was significantly increased in the HFD + Shanzha（Hawthorn）extract group compared to that in the HFD group, and there was no significant difference in the HFD + NETs inhibitor GSK484 group. Compared to those in the HFD group, in the HFD + Shanzha（Hawthorn）extract and HFD + NETs inhibitor GSK484 groups, the expression levels of MPO and CitH3 dropped significantly. The protein expressions of Tbx21 and RORγt decreased notably, while the Gata3 protein expression increased. Bcl-6 and Foxp3 in the HFD + Shanzha（Hawthorn）extract group increased significantly, but in the HFD + NETs inhibitor GSK484 group, Foxp3 showed no significant change.

The mechanism of action of Shanzha（Hawthorn）extract may be related to the regulation of factors such as Tbx21, RORγt and Gata3, which affect Th1/Th2 and Th17/Treg differentiation, by decreasing the level of NETs in dyslipidemic mice and thus effectively ameliorating dyslipidemia.

To investigate the inhibitory pharmacological effects of Morusin on the function of the RNA polymerase of SARS-CoV-2, and the target enzyme inhibitory activity of 5 kinds of traditional Chinese medicine ingredients similar to mulberry sinin was predicted.

Molecular docking technology was used to study the binding mode of Morusin to the active site of the RNA polymerase of SARS-CoV-2. The inhibitory activity of Morusin on RNA polymerase was then tested using a cell-based RNA polymerase catalytic system. Five small molecules with structural analogs of morocinin were selected from the components of Morus traditional Chinese medicine, and their interaction patterns with amino acids at the active site of RNA polymerase were studied using molecular docking methods.

Morusin can firmly occupy the NTPs channel of RNA polymerase and block the entry of nucleotides, thereby inhibiting the nucleic acid replication function of RNA polymerase. Pharmacological experiments at the cellular level confirmed that the inhibitory activity of Morusin on RNA polymerase was stronger than that of the control drug remdesivir. At the same time, the 5 kinds of small molecules of the structural analogs of mulberry can also bind to the active site of RNA polymerase and have enzyme inhibitory activity.

This study has found that Morusin has strong inhibitory activity on RNA polymerase, the five analogs are also predicted to have strong RNA polymerase inhibitory activity, and the results can provide a reference for the development of anti-SARS-CoV-2 drugs.

To observe the effects of Yiqi Huoxue Tiaomai Decoction（益气活血调脉汤）combined with amiodarone on rapid ventricular rate control and cardiac function in patients with atrial fibrillation.

Sixty patients with atrial fibrillation and rapid ventricular rate admitted to the Traditional Chinese Medicine Department of the hospital from January to December 2023 were selected. The patients were randomly divided into two groups using a digitalization method：a control group（taking amiodarone hydrochloride tablets orally, 30 cases）and an observation group（taking Yiqi Huoxue Tiaomai Decoction combined with amiodarone hydrochloride tablets orally, 30 cases）. The clinical efficacy, ventricular rate, heart function, and adverse reactions were compared between two groups.

The effective rate of the control group（73.33%）was significantly lower than that of the observation group（93.33%）, and the difference was statistically significant（P < 0.05）. There was no significant difference in ventricular rate between the two groups before and one week after intervention（P > 0.05）. After 2 weeks of intervention, the ventricular rate of the observation group decreased compared to that of the control group, but the difference was not statistically significant（P > 0.05）. After 3 and 4 weeks of intervention, the ventricular rate of the observation group patients was significantly reduced compared to that of the control group（P < 0.01）. There was no significant difference in the levels of various cardiac function indicators between the two groups before intervention（P > 0.05）. After 4 weeks of intervention, the levels of left ventricular ejection fraction（LVEF）and the ratio of peak early diastolic blood flow to peak late diastolic blood flow in the left ventricle（E/A）of the observation group were significantly increased compared to those of the control group, while the levels of left ventricular end diastolic diameter（LVEDD）and left ventricular end systolic diameter（LVESD）were significantly reduced（P < 0.01）. There was no significant difference in serum levels of angiotensin Ⅱ（Ang-Ⅱ）, norepinephrine（NE）or brain natriuretic peptide（BNP）between the two groups before intervention（P > 0.05）. After 4 weeks of intervention, the serum levels of Ang-Ⅱ, NE and BNP in the observation group were significantly lower than those in the control group（P < 0.01）. There was no significant difference in the scores of main symptoms such as palpitations, chest tightness, heart pain, shortness of breath or fatigue between the two groups before intervention（P > 0.05）. After 4 weeks of intervention, the scores of the above symptoms in the observation group were significantly lower than those in the control group（P < 0.01）. During the intervention period, the two groups experienced adverse reactions, mainly including gastrointestinal discomfort, abnormal liver and kidney function, abnormal bleeding and bradycardia, but there was no significant difference in the overall incidence rate（P > 0.05）.

The combination of Yiqi Huoxue Tiaomai Decoction and amiodarone in the treatment of patients with atrial fibrillation and rapid ventricular rate can not only control the heart rate, but also improve the cardiac function, alleviate the clinical symptoms such as palpitations, chest tightness, pain, shortness of breath and fatigue.

This study observed the effects of Jianpi Huatan Formula（健脾化痰方, JPHTF）on oxidized low-density lipoprotein（ox-LDL）induced vascular smooth muscle cell viability, proliferation, phenotype transformation and inflammatory factors in vitro.

Smooth muscle cells were isolated from the thoracic aorta of C57BL/6J mice. The 6-8 week old Sprague Dawley rats were orally administered, and the blood samples were collected from the abdominal aorta to prepare the drug containing serum. The DMEM medium culture was the control group. The ox-LDL induction（100 μg/mL）was the ox-LDL group. The atorvastatin group were the serum containing ox-LDL and atorvastatin（0.4 μM）. JPHTF low, middle and high dose groups were the serum containing ox-LDL and JPHTF（5%, 10%, 15%）. The identification of the first generation vascular smooth muscle cells？（VSMCs）was carried out by using immunofluorescence staining with α-smooth muscle actin（α-SMA）antibody. The cell counting kit-8（CCK-8）method was used to detect the cell viability. Transwell assay was used to observe the cell migration. Western Blot was used to detect the expressions of α-SMA, Calponin, SM22α, proliferating cell nuclear antigen（PCNA）, osteopontin（OPN）, ASC, NOD-like receptor family pyrin domain containing 3（NLRP3）and cleaved caspase-1 in cells, and enzyme-linked immunosorbent assay（ELISA）was used to detect the levels of interleukin-1β（IL-1β）, interleukin -18（IL-18）, tumor necrosis factor-α（TNF-α）and interleukin-6（IL-6）in cell supernatant.

JPHTF inhibited ox-LDL induced VSMCs proliferation and phenotype transition. JPHTF reduced the protein expression levels of NLRP3, ASC and cleaved caspase-1. ELISA results showed that JPHTF significantly reduced the levels of IL-1β and IL-18, as well as the levels of TNF-α and IL-6.

The effect of JPHTF in vitro can inhibit the conversion of VSMCs induced by ox-LDL from contractile phenotype to synthetic phenotype, reduce the ability of cell proliferation and migration, lower the levels of NL-RP3, ASC and cleaved caspase-1, and inhibit the activation of inflammasome, thereby inhibiting the development of atherosclerosis.

To reveal whether Formononetin（FMN）inhibits ferroptosis in HT22 cells induced by oxygen glucose deprivation/reoxygenation by activating the nuclear factor erythroid 2-related factor 2（Nrf2）/Glutathione peroxidase 4（GPX4）？pathway.

HT22 cells were subjected to oxygen-glucose deprivation/reoxygenation（OGD/R）damage to create an in vitro model, and HT22 cells were divided into control group（CON）, FMN group（FMN）, model group（OGD/R）, model + FMN group（OGD/R + FMN）, model + ML385 group（OGD/R + ML385）, model + RSL3 group（OGD/R + RSL3）. The CCK-8 method was used to detect the cell viability. DCFH-DA probe was used to detect the level of intracellular ROS. TUNEL staining and flow cytometry were used to detect the apoptosis. The colorimetric method was used to detect Fe²⁺ content in cells. Western blot was used to detect the protein expression levels of Nrf2 and GPX4.

Compared with those in the CON group, the cell proliferation activity in the OGD/R group was significantly reduced, the Fe²⁺ content, ROS level and apoptosis ratio were significantly increased, and the protein expressions of Nrf2 and GPX4 were significantly decreased（P > 0.05）. Compared with the OGD/R group, the OGD/R + FMN group had significantly increased cell proliferation activity（P < 0.05）, Fe²⁺ content, ROS level and apoptosis ratio significantly decreased and the expressions of Nrf2 and GPX4 proteins increased significantly. Compared with those of the OGD/R group, the cell proliferative activity of the OGD/R + ML385 group and the OGD/R + RSL3 group was significantly decreased（P < 0.05）, the Fe²⁺ content, ROS level and apoptosis ratio were significantly increased, the expression of Nrf2 protein in the OGD/R + ML835 group was significantly decreased（P < 0.05）, and the expression of GPX4 protein in the OGD/R + RSL3 group was significantly decreased（P < 0.05）.

FMN may inhibit ferroptosis induced by oxygen glucose deprivation/reoxygenation by activating the Nrf2/GPX4 pathway.

To explore the protective effect of Bushen Zhuanggu Prescription（补肾壮骨方）on chondrocyte degeneration in rats and its mechanism of action.

Primary chondrocytes from rats were isolated and stimulated with various concentrations of interleukin-1β（IL-1β）to identify the optimal concentration for inducing an osteoarthritis（OA）cell model. Concurrently, the serum containing Bushen Zhuanggu Formula at high, medium and low concentration gradients, or serum containing hydrochloric aminoglucose capsules, was prepared as a cellular intervention. The expressions of mRNA and proteins related to cartilage degeneration and the Wnt/β-catenin signaling pathway were measured, and the transmission electron microscopy was used to evaluate the changes in cellular ultrastructure.

After stimulation with IL-1β, the expressions of proteins related to cartilage degeneration and the Wnt/β-catenin pathway in chondrocytes was significantly abnormal, and the severe cellular damage was observed under ultrastructural examination. However, Bushen Zhuanggu Formula, by inhibiting the activation of the Wnt/β-catenin signaling pathway, reduced the expressions of inflammatory factors and MMPs induced by IL-1β and promoted the expressions of Collagen Ⅱ and Aggrecan, thereby protecting the chondrocytes.

Serum containing Bushen Zhuanggu Formula can reduce the abnormal expression of degeneration-related proteins by inhibiting the Wnt/β-catenin pathway, thus exerting a protective effect.