Kinsenoside is a main active component isolated from plants of the genus Anoectochilus,and exhibits many biological activities and pharmacological effects,including hepatoprotective,anti-hyperglycemic,anti-hyperliposi...Kinsenoside is a main active component isolated from plants of the genus Anoectochilus,and exhibits many biological activities and pharmacological effects,including hepatoprotective,anti-hyperglycemic,anti-hyperliposis,anti-inflammatory,vascular protective and anti-osteoporosis effects and so on,which is contributing to its promising potency in disease treatments.This review aims to recapitulate the pharmacological functions of kinsenoside,as well as its source,extraction,identification,quantitative analysis,pharmacokinetics,synthesis and patent information.The data reported in this work can confirm the therapeutic potential of kinsenoside and provide useful information for further new drug development.展开更多
The objective was to investigate the effect of kinsenoside(Kin) treatments on macrophage polarity and evaluate the resulting protection of chondrocytes to attenuate osteoarthritis(OA) progression.RAW264.7 macrophages ...The objective was to investigate the effect of kinsenoside(Kin) treatments on macrophage polarity and evaluate the resulting protection of chondrocytes to attenuate osteoarthritis(OA) progression.RAW264.7 macrophages were polarized to M1/M2 subtypes then administered with different concentrations of Kin. The polarization transitions were evaluated with quantitative real-time polymerase chain reaction(q RT-PCR), confocal observation and flow cytometry analysis. The mechanism of Kin repolarizing M1 macrophages was evaluated by Western blot. Further, macrophage conditioned medium(CM) and IL-1β were administered to chondrocytes. Micro-CT scanning and histological observations were conducted in vivo on anterior cruciate ligament transection(ACLT) mice with or without Kin treatment. We found that Kin repolarized M1 macrophages to the M2 phenotype. Mechanistically, Kin inhibited the phosphorylation of IκBα, which further reduced the downstream phosphorylation of P65 in nuclear factor-κB(NF-κB) signaling. Moreover, Kin inhibited mitogen-activated protein kinases(MAPK) signaling molecules p-JNK, p-ERK and p-P38. Additionally, Kin attenuated macrophage CM and IL-1β-induced chondrocyte damage. In vivo, Kin reduced the infiltration of M1 macrophages,promoted M2 macrophages in the synovium, inhibited subchondral bone destruction and reduced articular cartilage damage induced by ACLT. All the results indicated that Kin is an effective therapeutic candidate for OA treatment.展开更多
文摘Kinsenoside is a main active component isolated from plants of the genus Anoectochilus,and exhibits many biological activities and pharmacological effects,including hepatoprotective,anti-hyperglycemic,anti-hyperliposis,anti-inflammatory,vascular protective and anti-osteoporosis effects and so on,which is contributing to its promising potency in disease treatments.This review aims to recapitulate the pharmacological functions of kinsenoside,as well as its source,extraction,identification,quantitative analysis,pharmacokinetics,synthesis and patent information.The data reported in this work can confirm the therapeutic potential of kinsenoside and provide useful information for further new drug development.
基金supported by the National Natural Science Foundation of China(No.81672205)National Key R&D Programme(No.2016YFC1102100,China)the Shanghai Science and Technology Development Fund(Nos.18DZ2291200and 18441902700,China)
文摘The objective was to investigate the effect of kinsenoside(Kin) treatments on macrophage polarity and evaluate the resulting protection of chondrocytes to attenuate osteoarthritis(OA) progression.RAW264.7 macrophages were polarized to M1/M2 subtypes then administered with different concentrations of Kin. The polarization transitions were evaluated with quantitative real-time polymerase chain reaction(q RT-PCR), confocal observation and flow cytometry analysis. The mechanism of Kin repolarizing M1 macrophages was evaluated by Western blot. Further, macrophage conditioned medium(CM) and IL-1β were administered to chondrocytes. Micro-CT scanning and histological observations were conducted in vivo on anterior cruciate ligament transection(ACLT) mice with or without Kin treatment. We found that Kin repolarized M1 macrophages to the M2 phenotype. Mechanistically, Kin inhibited the phosphorylation of IκBα, which further reduced the downstream phosphorylation of P65 in nuclear factor-κB(NF-κB) signaling. Moreover, Kin inhibited mitogen-activated protein kinases(MAPK) signaling molecules p-JNK, p-ERK and p-P38. Additionally, Kin attenuated macrophage CM and IL-1β-induced chondrocyte damage. In vivo, Kin reduced the infiltration of M1 macrophages,promoted M2 macrophages in the synovium, inhibited subchondral bone destruction and reduced articular cartilage damage induced by ACLT. All the results indicated that Kin is an effective therapeutic candidate for OA treatment.
