In this paper,the pharmacological effects of aucubin include anti-inflammatory effect,anti-tumor effect,neuroprotective effect,anti-cardiovascular disease effect,hepatoprotective effect,anti-oxidation effect and anti-...In this paper,the pharmacological effects of aucubin include anti-inflammatory effect,anti-tumor effect,neuroprotective effect,anti-cardiovascular disease effect,hepatoprotective effect,anti-oxidation effect and anti-aging effect,antibacterial effect,anti-diabetes effect and bone protection.The purpose of this study is to provide theoretical basis for the development and clinical application of aucubin.展开更多
Hippocampal neuronal apoptosis accompanied by impairment of cognitive function occurs in primary diabetic encephalopathy. In this study, we investigated the neuroprotective mechanism of the iridoid glycoside, aucubin,...Hippocampal neuronal apoptosis accompanied by impairment of cognitive function occurs in primary diabetic encephalopathy. In this study, we investigated the neuroprotective mechanism of the iridoid glycoside, aucubin, using rats (n=8). Diabetes mellitus was induced in the rats by intraperitoneal (i.p.) injection of streptozotocin (60 mg/kg body weight). After 65 d, half of the DM rats were administered aucubin (5 mg/kg; i.p.) for 15 d, yielding treatment DM+A. A third group of rats received no strepto- zotocin or aucibin, and served as controls (CON). Encephalopathy was assessed using Y-maze be- havioral testing. Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) as- sessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apop- totic cell death. All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes.展开更多
Rheumatoid arthritis(RA)is a chronic inflammatory autoimmune disease.It is known that aucubin(AU)exerts anti-inflammatory activity,but its effects and mechanisms in RA are unclear.This study investigated the anti-infl...Rheumatoid arthritis(RA)is a chronic inflammatory autoimmune disease.It is known that aucubin(AU)exerts anti-inflammatory activity,but its effects and mechanisms in RA are unclear.This study investigated the anti-inflammatory effects and mechanisms of AU in vivo and in vitro.Human fibroblast-like synoviocyte cells from patients with RA(HFLS-RA),RAW264.7 cells,and MC3T3-E1 cells were used to evaluate the effects of AU on migration,invasion,apoptosis,osteoclast differentiation and production.Immunofluorescence was used to observe nuclear translocation of nuclear factor(NF)-/cB,the double luciferase reporter gene method was used to observe NF-/cB-p65 activity in AU-treated MC3T3-E1 cells.RT-qPCR was used to measure expression of bone metabolism and inflammation-related genes,and western blot was used to measure bone metabolism and NF-a:B protein expression levels.Collagen-induced arthritis(CIA)rat model was used for pharmacodynamics study.Arthritis indexes were measured in the ankle and knee,histological staining and Micro-computed tomography were performed on the ankle joints.Also,inflammatory factor gene expression and the levels of NF-/cB-related proteins were detected as in vitro.AU effectively inhibited HFLS-RA cell migration and invasion,promoted apoptosis,and inhibited RAW264.7 cell differentiation into osteoclasts,as well as inhibited NF-/cB-p65 activity in MC3T3-E1 cells.Notably,AU significantly reduced the gene expression levels of three cell-related inflammatory factors and bone metabolism factors,effectively inhibited the expression of p-lKKafi,p-lA:Ba,and p-p65 proteins.In vivo,AU relieved joint inflammation,reduced related inflammatory factors,and inhibited NF-/cB signaling.It could be used to treat RA-related synovial inflammation and bone destruction through the NF-/cB pathway.展开更多
基金Talent Training Program by the Central Government for the Reform and Development of Local Universities(2020GSP16)Innovation and Entrepreneurship Project for College Students(202110223003).
文摘In this paper,the pharmacological effects of aucubin include anti-inflammatory effect,anti-tumor effect,neuroprotective effect,anti-cardiovascular disease effect,hepatoprotective effect,anti-oxidation effect and anti-aging effect,antibacterial effect,anti-diabetes effect and bone protection.The purpose of this study is to provide theoretical basis for the development and clinical application of aucubin.
基金the National Natural Science Foundation of China (Grant No. 30371053)the National Outstanding Youth Foundation of China (Grant No. 30125034)the Scientific and Technological Plan Project of Dalian City (Grant No. 2003B3NS024)
文摘Hippocampal neuronal apoptosis accompanied by impairment of cognitive function occurs in primary diabetic encephalopathy. In this study, we investigated the neuroprotective mechanism of the iridoid glycoside, aucubin, using rats (n=8). Diabetes mellitus was induced in the rats by intraperitoneal (i.p.) injection of streptozotocin (60 mg/kg body weight). After 65 d, half of the DM rats were administered aucubin (5 mg/kg; i.p.) for 15 d, yielding treatment DM+A. A third group of rats received no strepto- zotocin or aucibin, and served as controls (CON). Encephalopathy was assessed using Y-maze be- havioral testing. Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) as- sessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apop- totic cell death. All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes.
基金This work was supported by the Natural Science Foundation of China(No.81773922)Shanghai Natural Science Foundation(No.19ZR1452000).
文摘Rheumatoid arthritis(RA)is a chronic inflammatory autoimmune disease.It is known that aucubin(AU)exerts anti-inflammatory activity,but its effects and mechanisms in RA are unclear.This study investigated the anti-inflammatory effects and mechanisms of AU in vivo and in vitro.Human fibroblast-like synoviocyte cells from patients with RA(HFLS-RA),RAW264.7 cells,and MC3T3-E1 cells were used to evaluate the effects of AU on migration,invasion,apoptosis,osteoclast differentiation and production.Immunofluorescence was used to observe nuclear translocation of nuclear factor(NF)-/cB,the double luciferase reporter gene method was used to observe NF-/cB-p65 activity in AU-treated MC3T3-E1 cells.RT-qPCR was used to measure expression of bone metabolism and inflammation-related genes,and western blot was used to measure bone metabolism and NF-a:B protein expression levels.Collagen-induced arthritis(CIA)rat model was used for pharmacodynamics study.Arthritis indexes were measured in the ankle and knee,histological staining and Micro-computed tomography were performed on the ankle joints.Also,inflammatory factor gene expression and the levels of NF-/cB-related proteins were detected as in vitro.AU effectively inhibited HFLS-RA cell migration and invasion,promoted apoptosis,and inhibited RAW264.7 cell differentiation into osteoclasts,as well as inhibited NF-/cB-p65 activity in MC3T3-E1 cells.Notably,AU significantly reduced the gene expression levels of three cell-related inflammatory factors and bone metabolism factors,effectively inhibited the expression of p-lKKafi,p-lA:Ba,and p-p65 proteins.In vivo,AU relieved joint inflammation,reduced related inflammatory factors,and inhibited NF-/cB signaling.It could be used to treat RA-related synovial inflammation and bone destruction through the NF-/cB pathway.
