Aim To explore the key components and mechanisms of Lizhong decoction in treating rats with cold-damp diarrhea based on network pharmacology,molecular docking technology and animal experiments.Methods By literature review and database collec-tion,the components of Lizhong decoction,therapeutic targets,and the mapping with diarrhea disease targets were conducted to construct an intersection target pro-tein-protein interaction network for screening core tar-gets,and GO and KEGG pathway enrichment analysis was performed to build an"active component-target-pathway"network,followed by molecular docking vali-dation.Forty-eight rats were randomly divided into the normal control group(K),model group(DG),Lizhong decoction group(LZDG),and Pulsatilla decoction group(BTDG).Subsequently,a rat cold-damp diar-rhea model was established using Senna combined with low-temperature high-humidity environment,and the rats were intervened with Lizhong decoction and Pul-satilla decoction.HE staining was used to detect path-ological changes in intestinal tissue,ELISA was em-ployed to measure the levels of peripheral blood IL-6,IL-10,IL-1 β,and TNF-α,and western blot was used to determine the expression of colon tight junction pro-teins.Results Network pharmacology initially identi-fied 125 compounds in Lizhong decoction,5 186 drug target components,438 disease targets,and 60"drug-disease"shared targets.GO and KEGG enrichment a-nalysis showed that signaling pathways such as IL-17 and TNF were highly enriched.Molecular docking in-dicated that the core components of the drug had good binding activity with corresponding key targets.Liz-hong decoction could effectively improve the clinical symptoms of rats with cold-damp diarrhea,and com-pared with the DG group,the diarrhea rate,diarrhea in-dex,and other related indicators also gradually de-creased to normal levels.Compared with the DG group,the LZDG group showed reduced inflammation levels and a recovery in energy metabolism levels.Conclusion It can regulate targets such as MMP9 and IL-17 signaling pathways through multi-components like Calycosin and formononetin to exert its therapeutic effect on cold-damp diarrhea.

Aim To explore the key components and mechanisms of Lizhong decoction in treating rats with cold-damp diarrhea based on network pharmacology,molecular docking technology and animal experiments.Methods By literature review and database collec-tion,the components of Lizhong decoction,therapeutic targets,and the mapping with diarrhea disease targets were conducted to construct an intersection target pro-tein-protein interaction network for screening core tar-gets,and GO and KEGG pathway enrichment analysis was performed to build an"active component-target-pathway"network,followed by molecular docking vali-dation.Forty-eight rats were randomly divided into the normal control group(K),model group(DG),Lizhong decoction group(LZDG),and Pulsatilla decoction group(BTDG).Subsequently,a rat cold-damp diar-rhea model was established using Senna combined with low-temperature high-humidity environment,and the rats were intervened with Lizhong decoction and Pul-satilla decoction.HE staining was used to detect path-ological changes in intestinal tissue,ELISA was em-ployed to measure the levels of peripheral blood IL-6,IL-10,IL-1 β,and TNF-α,and western blot was used to determine the expression of colon tight junction pro-teins.Results Network pharmacology initially identi-fied 125 compounds in Lizhong decoction,5 186 drug target components,438 disease targets,and 60"drug-disease"shared targets.GO and KEGG enrichment a-nalysis showed that signaling pathways such as IL-17 and TNF were highly enriched.Molecular docking in-dicated that the core components of the drug had good binding activity with corresponding key targets.Liz-hong decoction could effectively improve the clinical symptoms of rats with cold-damp diarrhea,and com-pared with the DG group,the diarrhea rate,diarrhea in-dex,and other related indicators also gradually de-creased to normal levels.Compared with the DG group,the LZDG group showed reduced inflammation levels and a recovery in energy metabolism levels.Conclusion It can regulate targets such as MMP9 and IL-17 signaling pathways through multi-components like Calycosin and formononetin to exert its therapeutic effect on cold-damp diarrhea.

Medical institutions, with their clinical practice foundation and abundant human use experience data, have become important carriers for the inheritance and innovation of traditional Chinese medicine(TCM) and the "cradles" of the preparation of new TCM. To effectively promote the transformation of new TCM originating from the TCM clinical practice in medical institutions and establish an effective evaluation index system for the transformation of new TCM conforming to the characteristics of TCM, consensus experts adopted the literature research, questionnaire survey, Delphi method, etc. By focusing on the policy and technical evaluation of new TCM originating from the TCM clinical practice in medical institutions, a comprehensive evaluation from the dimensions of drug safety, efficacy, feasibility, and characteristic advantages was conducted, thus forming a comprehensive evaluation system with four primary indicators and 37 secondary indicators. The expert consensus reached aims to encourage medical institutions at all levels to continuously improve the high-quality research and development and transformation of new TCM originating from the TCM clinical practice in medical institutions and targeted at clinical needs, so as to provide a decision-making basis for the preparation, selection, cultivation, and transformation of new TCM for medical institutions, improve the development efficiency of new TCM, and precisely respond to the public medication needs.
Medicine, Chinese Traditional/standards* ; Humans ; Consensus ; Drugs, Chinese Herbal/therapeutic use* ; Surveys and Questionnaires

Aim To investigate the inhibitory effect of the protein kinase D(PKD)-specific inhibitor CRT0066101 on hepatocellular carcinoma(HCC)and its underlying molecular mechanisms,providing new theoretical insights and therapeutic strategies for targe-ted HCC treatment.Methods HCC cell lines were treated with varying concentrations of CRT0066101.The inhibitory effects on cell proliferation were assessed using the CCK-8 assay,colony formation assay,and EdU staining.The impact on cell migration and inva-sion was evaluated through wound-healing assays and Transwell migration and invasion assays.was employed toThe effects of CRT0066101 on the phosphorylation levels of PKD and key proteins in the downstream PI3K/AKT signaling pathway were analyzed using Western blot.Additionally,the drug's regulatory effects on apoptosis and autophagy in HCC cells were examined using Western blot,flow cytometry,and the mRFP-GFP-LC3 dual-fluorescence reporter system.Results CRT0066101 significantly inhibited the pro-liferation,migration and invasion of HCC cells.West-ern blotting results demonstrated that CRT0066101 dose-dependently suppressed the phosphorylation of PKD family proteins and downregulated the activation of the PI3K/AKT signaling pathway.Furthermore,CRT0066101 treatment upregulated the expression of the pro-apoptotic protein Bax while downregulating the anti-apoptotic protein Bcl-2.It also markedly increased the expression levels of autophagy marker proteins Bec-lin-1 and LC3B-Ⅱ,suggesting that the drug simulta-neously induced apoptosis and autophagy in HCC cells.Conclusions CRT0066101 specifically inhibits PKD activity,blocks the PI3K/AKT signaling path-way,suppresses HCC cell proliferation and metastasis,and induces apoptosis and autophagy.These findings indicate that CRT0066101 is a promising small-mole-cule inhibitor for targeted HCC therapy with potential clinical applications.

Aim To investigate the inhibitory effect of the protein kinase D(PKD)-specific inhibitor CRT0066101 on hepatocellular carcinoma(HCC)and its underlying molecular mechanisms,providing new theoretical insights and therapeutic strategies for targe-ted HCC treatment.Methods HCC cell lines were treated with varying concentrations of CRT0066101.The inhibitory effects on cell proliferation were assessed using the CCK-8 assay,colony formation assay,and EdU staining.The impact on cell migration and inva-sion was evaluated through wound-healing assays and Transwell migration and invasion assays.was employed toThe effects of CRT0066101 on the phosphorylation levels of PKD and key proteins in the downstream PI3K/AKT signaling pathway were analyzed using Western blot.Additionally,the drug's regulatory effects on apoptosis and autophagy in HCC cells were examined using Western blot,flow cytometry,and the mRFP-GFP-LC3 dual-fluorescence reporter system.Results CRT0066101 significantly inhibited the pro-liferation,migration and invasion of HCC cells.West-ern blotting results demonstrated that CRT0066101 dose-dependently suppressed the phosphorylation of PKD family proteins and downregulated the activation of the PI3K/AKT signaling pathway.Furthermore,CRT0066101 treatment upregulated the expression of the pro-apoptotic protein Bax while downregulating the anti-apoptotic protein Bcl-2.It also markedly increased the expression levels of autophagy marker proteins Bec-lin-1 and LC3B-Ⅱ,suggesting that the drug simulta-neously induced apoptosis and autophagy in HCC cells.Conclusions CRT0066101 specifically inhibits PKD activity,blocks the PI3K/AKT signaling path-way,suppresses HCC cell proliferation and metastasis,and induces apoptosis and autophagy.These findings indicate that CRT0066101 is a promising small-mole-cule inhibitor for targeted HCC therapy with potential clinical applications.

Tranexamic acid is widely used in joint orthopedic surgery.At the same time,it has high safety and few adverse drug reactions.It can effectively improve intraoperative bleeding and promote early functional recovery of patients.This article reviews the mode of administration,safe dose,administration time and adverse drug reactions of tranexamic acid in the perioperative period of joint replacement and arthroscopic surgery,in order to provide reference for the clinical application of tranexamic acid.

Investigating the structural characteristics of proton tautomers is of great significance for understanding organic reactions and biochemical processes.In this study,a method based on ion mobility mass spectrometry combined with ab initio molecular dynamics calculations was proposed.The structures of proton tautomers were determined by comparing the experimental and theoretical collision-induced dissociation(CID)mass spectrograms of different proton tautomers.Ion mobility mass spectrometry was used to separate proton tautomerism produced during ionization.The CID mass spectra of each isomer could be obtained after mobility separation.The quantum chemical mass spectrometry(QCXMS)program based on ab initio molecular dynamics calculations was used to calculate the fragmentation process and obtain the theoretical CID mass spectra.The results of experiment and calculation showed that this method effectively solved the issue of difficult identification of proton tautomers.This method was also of great significance for the study of ionization mechanism and organic reaction process using mass spectrometry.

COVID-19 has been prevalent for three years. The virulence of SARS-CoV-2 is weaken as it mutates continuously. However, elderly patients, especially those with underlying diseases, are still at high risk of developing severe infections. With the continuous study of the molecular structure and pathogenic mechanism of SARS-CoV-2, antiviral drugs for COVID-19 have been successively marketed, and these anti-SARS-CoV-2 drugs can effectively reduce the severe rate and mortality of elderly patients. This article reviews the mechanism, clinical medication regimens, drug interactions and adverse reactions of five small molecule antiviral drugs currently approved for marketing in China, so as to provide advice for the clinical rational use of anti-SARS-CoV-2 in the elderly.

Aim To study the effect of sodium pyruvate on apoptosis and autophagy of HT22 in mouse hippocampal neuronal cells under hypoxia conditions. Methods HT22 cells were incubated with different concentrations of sodium pyruvate to detect their cellular activity by MTS; iron staining was used to further observe the effect of sodium pyruvate on HT22 cells in mitochondrial metabolism; lysosomal staining was applied to detect the lysosomal changes of sodium pyruvate on HT22 cells; Western blot was used to detect the expression of Bcl-2, Bax and LC3-II/LC3- I proteins. Results To verify whether sodium pyruvate exerted neuroprotective effects on mouse hippocampal HT22 cells through affecting mitochondrial apoptosis and autophagy pathways, which were improved by administration of sodium pyruvate. Conclusions Sodium pyruvate administration under hypoxic conditions can reduce the neuroprotective effect of hypoxic injury by reducing apoptosis and activating autophagy in HT22 cells.

OBJECTIVE: To evaluate the associations of lipid indicators and mortality in Beijing Elderly Comprehensive Health Cohort Study. METHODS: A prospective cohort was conducted based on Beijing Elderly Comprehensive Health Cohort Study with 4499 community older adults. After the baseline survey, the last follow-up was March 31, 2021 with an average 8.13 years of follow-up. Cox proportional hazard model was used to estimate the hazard ratios (HR) with 95% CI for cardiovascular disease (CVD) death and all-cause death in associations with baseline lipid indicators. RESULTS: A total of 4499 participants were recruited, and the mean levels of uric acid, body mass index, systolic blood pressure, diastolic blood pressure, fasting plasma glucose, total cholesterol (TC), triglyceride, and low-density lipoprotein cholesterol (LDL-C) showed an upward trend with the increasing remnant cholesterol (RC) quarters (P_trend < 0.05), while the downward trend was found in high-density lipoprotein cholesterol (HDL-C). During the total 36,596 person-years follow-up, the CVD mortality and all-cause mortality during an average 8.13 years of follow-up was 3.87% (95% CI: 3.30%-4.43%) and 14.83% (95% CI: 13.79%-15.86%) with 174 CVD death participants and 667 all-cause death participants. After adjusting for confounders, the higher level of TC (HR = 0.854, 95% CI: 0.730-0.997), LDL-C (HR = 0.817, 95% CI: 0.680-0.982) and HDL-C (HR = 0.443, 95% CI: 0.271-0.724) were associated with lower risk of CVD death, and the higher level of HDL-C (HR = 0.637, 95% CI: 0.501-0.810) were associated with lower risk of all-cause death. The higher level of RC (HR = 1.276, 95% CI: 1.010-1.613) increase the risk of CVD death. Compared with the normal lipid group, TC ≥ 6.20 mmol/L group and LDL-C ≥ 4.10 mmol/L group were no longer associated with lower risk of CVD death, while RC ≥ 0.80 mmol/L group was still associated with higher risk of CVD death. In normal lipid group, the higher levels of TC, LDL-C and HDL-C were related with lower CVD death. CONCLUSIONS In community older adults, higher levels of TC and HDL-C were associated with lower CVD mortality in normal lipid reference range. Higher RC was associated with higher CVD mortality, which may be a better lipid indicator for estimating the CVD death risk in older adults.