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.

It is believed that psoriasis with anxiety and depression presents the pathogenesis of "depression-blood-spirit"， with qi depression as the initiating factor， and that the disease mechanism is understood from three aspects， including "qi depression transforming into fire， blood stasis disturbing the spirit"， "depressed fire consuming yin， causing blood dryness and spirit agitation"， "qi stagnation leading to blood stasis， resulting in obstructed channels and spirit depression". The treatment proposes three methods， firstly， cooling blood and resolving depression， secondly， nourishing blood and soothing depression， and thirdly， activating blood and regulating depression， which applies prescriptions as modified Liangxue Huoxue Decoction （凉血活血汤） combined with Zhiqiao （Poncirus trifoliata）， Foshou （Citrus medica）， and Lianqiaoxin （Forsythia suspensa） for cooling blood and resolving depression； modified Yangxue Jiedu Decoction （养血解毒汤） combined with Baishao （Paeonia lactiflora Pall）， Zhenzhumu （Margaritifera Concha）， and calcined Muli （Ostreidae） for nourishing blood and soothing depression； and modified Huoxue Sanyu Decoction （活血散瘀汤） combined with Yujin （Curcuma aromatica） and Hehuanpi （Albiziae Cortex） for activating blood and regulating depression. These three methods integrate the "depression-blood-spirit" pathogenesis to achieve harmony of body and spirit by clearing blood heat， nourishing yin and blood， and removing blood stasis， complemented with medicinals that soothing the liver， calming the spirit， and regulating depression.

OBJECTIVE: Peritoneal dialysis(PD)-associated peritonitis is a common and major complication of PD and the most common cause of technical failure of PD. The presence of bacterial biofilm may be an important factor leading to refractory or recurrence of peritonitis. To investigate the formation and characteristics of bacterial biofilms on PD catheters after peritonitis-associated catheter removal. METHODS: The patients with maintenance PD who were regularly followed up in the Peking University People' s Hospital from June 2007 to January 2022 were retrospectively analyzed. The patients who withdrew from PD because of peritonitis and removed the PD catheter in our hospital and underwent the scanning electron microscope examination of the catheter were selected. The general information of the patients, the electron microscope results of the PD catheter and the bacterial culture results of the PD fluid were summarized. RESULTS: (1) A total of 18 patients were included, 11 were female (accounting for 61.1%). The average age of the patients was (59.1±11.5) years, and the average duration of dialysis was (80.1±47.4) months. Primary kidney diseases were predominantly chronic glomerulonephritis (55.6%), followed by diabetic nephropathy (27.8%), and others (16.6%). The reasons for catheters removal in 18 patients were refractory peritonitis in 11 cases, recurrent peritonitis in 5 cases, and fungal peritonitis in 2 cases. (2) 16 of the 18 patients (88.9%) had catheter bacterial biofilm, and the bacterial biofilm forms were all cocci. Some were arranged in grape-like shapes, and their diameters ranged from about 500 nm to 1 000 nm. The bacterial culture results of peritoneal dialysis fluid showed that the three most common pathogens were Escherichia coli, methicillin-sensitive Staphylococcus aureus (MSSA), and Staphylococcus epidermidis. (3) Among the 18 patients enrolled, 13 patients (72.2%) had peritonitis in the past. The causative bacteria of peritonitis in 9 patients were cocci, including coagulase-negative Staphylococci (Staphylococcus suis, Staphylococcus surface, Staphylococcus xylosus, Staphylococcus warneri), Staphylococcus aureus, Streptococcus (Streptococcus salivarius and Aerococus viridans). CONCLUSION Bacterial biofilm formation on the inner surface of PD catheter is common in peritonitis-associated catheter removal patients. Not all PD catheters removed due to peritonitis have bacterial biofilms. Bacterial biofilms and peritonitis pathogens may not be consistent.
Humans ; Biofilms/growth & development* ; Peritonitis/etiology* ; Peritoneal Dialysis/instrumentation* ; Middle Aged ; Female ; Male ; Retrospective Studies ; Catheters, Indwelling/microbiology* ; Device Removal ; Catheter-Related Infections/microbiology* ; Aged ; Adult

Coptis chinensis Franch. and Panax ginseng C. A. Mey. are traditional herbal medicines with millennia of documented use and broad therapeutic applications, including anti-diabetic properties. However, the synergistic effect of total alkaloids from Coptis chinensis and total ginsenosides from Panax ginseng on type 2 diabetes mellitus (T2DM) and its underlying mechanism remain unclear. The research demonstrated that the optimal ratio of total alkaloids from Coptis chinensis and total ginsenosides from Panax ginseng was 4∶1, exhibiting maximal efficacy in improving insulin resistance and gluconeogenesis in primary mouse hepatocytes. This combination demonstrated significant synergistic effects in improving glucose tolerance, reducing fasting blood glucose (FBG), the weight ratio of epididymal white adipose tissue (eWAT), and the homeostasis model assessment of insulin resistance (HOMA-IR) in leptin receptor-deficient (db/db) mice. Subsequently, a T2DM liver-specific network was constructed based on RNA sequencing (RNA-seq) experiments and public databases by integrating transcriptional properties of disease-associated proteins and protein-protein interactions (PPIs). The network recovery index (NRI) score of the combined treatment group with a 4∶1 ratio exceeded that of groups treated with individual components. The research identified that activated adenosine 5'-monophosphate-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling in the liver played a crucial role in the synergistic treatment of T2DM, as verified by western blot experiment in db/db mice. These findings demonstrate that the 4∶1 combination of total alkaloids from Coptis chinensis and total ginsenosides from Panax ginseng significantly improves insulin resistance and glucose and lipid metabolism disorders in db/db mice, surpassing the efficacy of individual treatments. The synergistic mechanism correlates with enhanced AMPK/ACC signaling pathway activity.
Animals ; Panax/chemistry* ; Ginsenosides/administration & dosage* ; Diabetes Mellitus, Type 2/metabolism* ; Mice ; Male ; Alkaloids/pharmacology* ; Coptis/chemistry* ; Drug Synergism ; Insulin Resistance ; Mice, Inbred C57BL ; Humans ; Transcriptome/drug effects* ; Blood Glucose/metabolism* ; Hypoglycemic Agents/administration & dosage* ; Drugs, Chinese Herbal/administration & dosage* ; Hepatocytes/metabolism*

Cerebral organoids are three-dimensional nerve cultures induced by embryonic stem cells(ESCs)or induced pluripotent stem cells(iPSCs)that mimic the structure and function of human brain.With the continuous optimization of cerebral organoid culture technology and the combination with emerging technologies such as organ transplantation,gene editing and organoids-on-chip,complex brain tissue structures such as functional vascular structures and neural circuits have been produced,which provides new methods and ideas for studying human brain development and diseases.This article reviews the latest advances in brain organoid technology,describes its application in neurological diseases and advances in stroke modeling and transplantation treatment.

Post-stroke cognitive impairment(PSCI)is mainly manifested as learning and memory disorders.Highly enriched RNA m6A methylation modification in mammalian brain is involved in glial cell-mediated neuroinflammation.Given that neuroinflammation is the main mechanism for neural damage and spatial and memory impairment of PSCI,it is speculated that RNA m6A methylation modification can regulate the inflammatory response of glial cells after stroke to improve PSCI.This review summarizes and analyzes the role of RNA m6A methylation modification in the development of PSCI and analyzes its detailed mechanism of regulating glial cell-mediated inflammation,which will provide reference for researchers in this field.