Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Objective:To investigate the risk factors of colorectal adenomatous polyps.Methods:The clinical data of 395 patients who underwent colonoscopy in the Tongzhou branch, Tongzhou District, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine from August 2017 to August 2021 were analyzed. According to the examination results, adenomatous polyps were divided into adenomatous polyps group (193 cases) and non-polyp group (202 cases). The risk factors of colorectal adenomatous polyps were screened by univariate analysis and multivariate logistic regression analysis.Results:The results of single factor analysis suggested that: body mass index (BMI), sex, age, proportion of blood type A, history of large intestine polyps, history of Helicobacter pylori (Hp) infection, history of alcohol consumption, history of smoking, proportion of heavy oil diet, history of oral calcium, history of oral statins, history of oral non-steroidal anti-inflammatory drugs, history of oral antibiotics, and high fat diet (pork, beef, and animal organs), high salt diet, love of pickled food, love of sweet food, love of greasy, good mood, anxiety, depression, impatience and irritability, history of hypertension, diabetes and hyperlipidemia were statistically significant in the adenomatous polyp group and the non-polyp group (all P<0.05). Factors with P<0.05 in the above single factor analysis were taken as independent variables, and the incidence of disease was taken as dependent variable for multi-factor logistic regression analysis. The results showed that BMI, age, blood type A, Hp infection history, drinking history, smoking history, oral non-steroidal anti-inflammatory drugs history, oral antibiotics history, high salt diet, good mood, hypertension were the influencing factors for the incidence of adenomatous polyps (all P<0.05). Conclusions:High BMI, old age, blood type A, history of Hp infection, smoking history, oral non-steroidal anti-inflammatory drug history, oral antibiotics history, high salt diet and hypertension are risk factors for the development of adenomatous polyps. Drinking alcohol and good mood can reduce the risk of colorectal adenomatous polyps. Therefore, targeted intervention measures can be formulated for high-risk patients to reduce the risk of colorectal adenomatous polyps.

Objective:To investigate the risk factors of colorectal adenomatous polyps.Methods:The clinical data of 395 patients who underwent colonoscopy in the Tongzhou branch, Tongzhou District, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine from August 2017 to August 2021 were analyzed. According to the examination results, adenomatous polyps were divided into adenomatous polyps group (193 cases) and non-polyp group (202 cases). The risk factors of colorectal adenomatous polyps were screened by univariate analysis and multivariate logistic regression analysis.Results:The results of single factor analysis suggested that: body mass index (BMI), sex, age, proportion of blood type A, history of large intestine polyps, history of Helicobacter pylori (Hp) infection, history of alcohol consumption, history of smoking, proportion of heavy oil diet, history of oral calcium, history of oral statins, history of oral non-steroidal anti-inflammatory drugs, history of oral antibiotics, and high fat diet (pork, beef, and animal organs), high salt diet, love of pickled food, love of sweet food, love of greasy, good mood, anxiety, depression, impatience and irritability, history of hypertension, diabetes and hyperlipidemia were statistically significant in the adenomatous polyp group and the non-polyp group (all P<0.05). Factors with P<0.05 in the above single factor analysis were taken as independent variables, and the incidence of disease was taken as dependent variable for multi-factor logistic regression analysis. The results showed that BMI, age, blood type A, Hp infection history, drinking history, smoking history, oral non-steroidal anti-inflammatory drugs history, oral antibiotics history, high salt diet, good mood, hypertension were the influencing factors for the incidence of adenomatous polyps (all P<0.05). Conclusions:High BMI, old age, blood type A, history of Hp infection, smoking history, oral non-steroidal anti-inflammatory drug history, oral antibiotics history, high salt diet and hypertension are risk factors for the development of adenomatous polyps. Drinking alcohol and good mood can reduce the risk of colorectal adenomatous polyps. Therefore, targeted intervention measures can be formulated for high-risk patients to reduce the risk of colorectal adenomatous polyps.

Objective To collect and sort out the literature on the clinical medication experience of traditional Chinese medicine(TCM)in the treatment of hepatic precancerous lesions,and to summarize the characteristics of the disease and the treatment ideas by analyzing the rules of its formula,in order to provide instructions for the treatment of precancerous lesions of hepatocellular carcinoma with TCM in terms of medication and experience addition and subtraction.Methods CNKI,VIP,WanFang Data,CBM,PubMed,Web of Science,EMBASE,Cochrane databases were systematically searched,the clinical research and personal experience literature of TCM in the treatment of hepatic precancerous lesions from the establishment of the databases to December 2023 was included,and the prescription information that met the inclusion criteria was extracted.Based on"Traditional Chinese Medicine data Miner(TCM Miner)",the medication database was established to analyze the frequency,properties and flavours of the drugs and meridian tropism.The cluster analysis were conducted by SPSS 25.0 statistical software,and the association rules were analyzed by using Apriori algorithm of SPSS Modeler 14.1,and the complex network analysis of high-frequency drugs was conducted by network module of SPSS Modeler.Results 34 researches including 34 formulas,110 drugs with 291 frequencies and 15 drug efficacy were included.Frequency analysis showed that the top eight types of frequently applied drugs were milkvetch root,largehead atractylodes rhizome,radix salviae miltiorrhhizae,hedyotis,carapax trionycis,zedorgy rhidoray,barbated skullcup herb,redix curcumae.The top three properties in the"four qi"were cold,warm and mild.The top three tastes of the"five flavors"were bitterness,sweetness and acridity.The top four in the frequency of meridian tropism were liver,spleen,kidney and lung.Apriori correlation analysis showed that the core drug pairs was"Hedyotis diffusa+Atractylodes".Complex network analysis showed that the core prescriptions were composed of Atractylodes,Radix Paeoniae Alba,Hedyotis diffusa,Poria cocos,Rhizoma Curcumae,Radix Curcumae Aromaticae,Trionycis Carapax,Radix Astragali,Sparganium stoloniferum,Salvia miltiorrhiza,Scutellaria barbata.Conclusion The TCM treatment of hepatic precancerous lesions should be based on tonifying spleen and nourishing liver,promoting blood circulation and detoxification,and combined with drugs that can promote qi-circulation,clear heat,remove blood-stasis,soften hard masses and resolve hard masses.

Objective:To explore the effects of neonatal stimulator of interferon genes (STING) innate immune signaling pathway of HBsAg-positive mothers on non/hypo-response to hepatitis B vaccine (HepB) in their infants.Methods:From November 2019 to June 2022, HBsAg-positive mothers and their infants in the Third People's Hospital of Taiyuan were recruited as the study subjects. The epidemiological and clinical data were collected by questionnaire survey and medical records review. The key molecular proteins of STING innate immune signaling pathway (STING, pIRF3) and immune cells associated with vaccine response (DC, T and B and plasma cells) in neonatal cord blood were detected by flow cytometry. Follow up was conducted for infants for 1-2 months after the full vaccination of HepB. Serum hepatitis B surface antibody (anti-HBs) was detected by chemiluminescence microparticle immunoassay. Unconditional logistic regression model, nomogram and Bayesian network model were used to evaluate the effect of STING innate immune signaling pathway on non/hypo-response to HepB and related factors in infants, and the relationship between various factors.Results:A total of 195 pairs of HBsAg-positive mothers and infants were recruited, the rate of non/hypo-response to HepB in the infants was 12.31% (24/195). High maternal HBV DNA load, low expression of neonatal STING, low expression of pIRF3 and low percentage of plasma cells were risk factors for non/hypo-response to HepB in the infants ( OR=4.70, 3.46, 3.18 and 2.20, all P<0.05). The nomogram constructed by these factors had good predictive efficacy (area under curve=0.81, 95% CI: 0.63-0.83). The results of Bayesian network model showed that the infants with a high maternal HBV DNA load had a higher conditional probability of low STING expression (62.50%) and a higher conditional probability of low pIRF3 expression (58.54%). The conditional probabilities of low expression of DC, T, B and plasma cells were 53.16%, 60.20%, 68.42% and 57.14%, respectively. Conclusion:Maternal HBV DNA might inhibit STING innate immune signaling pathways in infants and immune cells associated with HepB response, resulting in non/hypo-response to HepB in infants of HBsAg-positive mothers.

Objective:To investigate the effect of liraglutide(LRG) on high glucose-induced oxidative stress injury in(H9c2) cardiomyocytes and its underlying mechanisms.Methods:A high glucose treatment was applied to H9c2 cells for 24 hours to establish an in vitro model of myocardial cell injury. Different concentrations of liraglutide(10, 100, 1000 nmol/L) were administered for intervention. Cell viability was evaluated using the CCK-8 assay, and changes in cell morphology were observed under an inverted microscope. After 24 hours of liraglutide(100 nmol/L) intervention following high glucose treatment, the levels of lactate dehydrogenase(LDH), superoxide dismutase(SOD), and malondialdehyde(MDA) in the cell supernatant were measured. RT-PCR and Western blotting were used to detect the mRNA and protein levels of silent information regulator factor 1(SIRT1) and forkhead box protein O1(FOXO1). Western blotting was also used to assess the acetylation level of FOXO1 protein. Small interfering RNA(siRNA) technology was employed to silence SIRT1 in H9c2 cells to confirm its role in the study. Results:Compared to the control group, the high glucose group showed decreased cell viability, cell structure damage, increased levels of LDH and MDA in the cell supernatant, decreased SOD levels, aggravated oxidative stress, decreased SIRT1 expression, and increased acetylation level of FOXO1(all P<0.05). Compared to the high glucose group, liraglutide intervention resulted in increased cell viability, improved cardiac cell morphology, reduced oxidative stress levels, increased SIRT1 expression, and decreased acetylation level of FOXO1(all P<0.05). When SIRT1 was downregulated, the protective effects of liraglutide were weakened(all P<0.05). Conclusions:Liraglutide has a protective effect against high glucose-induced oxidative stress injury in H9c2 cells, which may be associated with the upregulation of SIRT1 expression.