Astragaloside IV attenuates Toll-like receptor 4 expression via NF-κB pathway under high glucose condition in mesenchymal stem cells

Li, Mincai; Yu, Liangzu; She, Tonghui; Gan, Yapin; Li, Fuxin; Hu, Zhengwu; Chen, Yongbin; Li, Suqin; Xia, Hongli

doi:10.1016/j.ejphar.2012.09.033

Cited by 36 publications

(26 citation statements)

References 30 publications

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“…Cell viability was also impacted by bupivacaine and enhanced by glucose pretreatment. It is possible that decreased cell viability and increased apoptotic rate are due to increased proliferation rates, but our result demonstrated that high glucose magnified the proliferation‐inhibition effect of bupivacaine, which is consistent with previous research (Li et al, ; Lucchinetti et al, ). Apoptosis is a biological process regulated by multiple signaling cascades, which ultimately results in biochemical and morphological alterations in apoptotic cells.…”

Section: Discussionsupporting

confidence: 93%

Hyperglycemia magnifies bupivacaine‐induced cell apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress

et al. 2013

J of Neuroscience Research

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Nerve cell injury associated with apoptosis plays an important role in the development of diabetic peripheral neuropathy (DPN). However, it remains unclear whether preexisting or potential neurocyte damage induced by hyperglycemia increases sensitivity to local anesthetics. SH-SY5Y cells were pretreated with a high concentration of glucose in vitro, to imitate DPN prior to administration of bupivacaine or placebo. Cell viability and apoptosis were investigated with a CCK-8 assay and flow cytometry, respectively. In addition, mitochondrial membrane potential, reactive oxygen species (ROS), mitochondrially generated ROS, and activity of mitochondrial complexes I and III were studied to explore the molecular mechanism of bupivacaine-induced mitochondrial injury. Grp78 and caspase-12 expression were measured by qRT-PCR and Western blot, representing endoplasmic reticulum (ER) stress. Cell structure was also assessed via transmission electron microscopy. Incubation with bupivacaine decreased the activity of mitochondrial complexes I and III; increased ROS production at cell and mitochondrial levels, mitochondrial potential depolarization, and Grp78 and caspase-12 expression at both transcription and translation levels; and affected cell structure, which could be enhanced by glucose pretreatment. These findings indicate that mitochondrial dysfunction and ER stress related to ROS are involved in bupivacaine-induced apoptosis and may be enhanced by glucose administration.

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Section: Discussionsupporting

confidence: 93%

Hyperglycemia magnifies bupivacaine‐induced cell apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress

et al. 2013

J of Neuroscience Research

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“…Pharmacological activities attributed to AS-IV include cardioprotective (21), anti-inflammatory (22), antioxidant (23), anti-asthmatic (24) and anticancer (25) effects. Some of these pharmacological activities resulted from AS-IV-mediated inhibition of ERK (26)(27)(28) and NF-κB (26,(29)(30)(31) signaling pathways. Furthermore, AS-IV has been reported to affect osteogenesis (32), and have anti-arthritis activity (33).…”

Section: Inhibition Of Rankl-induced Osteoclastogenesis Through the Smentioning

confidence: 99%

Inhibition of RANKL-induced osteoclastogenesis through the suppression of the ERK signaling pathway by astragaloside IV and attenuation of titanium-particle-induced osteolysis

Wang

Geng

et al. 2015

International Journal of Molecular Medicine

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Astragaloside IV (AS-IV) is a natural plant extract that enhances osteoblast activity, and therefore, has the potential to treat osteoclast‑related diseases. Such diseases include osteoporosis, periodontal disease, rheumatoid arthritis and aseptic prosthesis loosening. However, data associating the effects of AS‑IV on osteoclasts are limited. The aim of the present study was to assess the effect of AS‑IV on osteoclasts in vitro and in vivo. The in vitro studies demonstrated that AS‑IV exerts potent inhibitory effects on the ligand of the receptor activator of nuclear factor‑κB‑induced osteoclastogenesis and revealed the mechanism of action of AS‑IV, which inhibited osteoclastogenesis by suppression of the extracellular signal‑regulated kinase signaling pathway. The in vivo studies proved that AS‑IV attenuated titanium particle‑induced osteolysis in a mouse calvarial model. Collectively, the findings of the study suggest that AS‑IV is a potential natural agent for the treatment of osteoclast-related diseases.

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“…Bge. is one of the major and active components of Αstragalus membranaceus , which has been shown to have comprehensive pharmacological function ( 17 , 18 ). Diverse pharmacological activities have been found to be exerted by AS-IV such as anti-inflammatory, anti-oxidation, anti-infarction and antinociception ( 19 – 21 ).…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV ameliorates acute pancreatitis in rats by inhibiting the activation of nuclear factor-κB

Qiu

Guo

Cheng

et al. 2015

International Journal of Molecular Medicine

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This study aimed to investigate the effects of astragaloside IV (AS-IV; 3-O-β-D-xylopyranosyl-6-O-β-D-glucopyranosylcycloastragenol), which has been reported to have comprehensive pharmacological functions, on sodium taurocholate (NaTc)/L-arginine (L-Arg)-induced acute pancreatitis (AP) in rats in vivo and in rat pancreatic acinar cells in vitro. NaTc-induced experimental AP was induced in rats by injecting 4% NaTc (0.1 ml/100 g) in the retrograde direction of the biliopancreatic duct. L-Arg-induced experimental AP was induced in rats by 2 intraperitoneal injections of 20% L-arg (3 g/kg), with an interval of 1 h between the injections. The rats were pre-treated AS-IV (50 mg/kg) or the vehicle (DMSO) 2 h prior to the induction of AP. Enzyme-linked immunosorbent assay, H&E staining, myeloperoxidase (MPO) activity, reverse transcription-quantitative PCR, western blot analysis and immunohistochemistry were used to evaluate the effects of AS-IV on AP. The results revealed that treatment with AS-IV significantly reduced serum amylase and lipase levels, pancreatic pathological alterations, the secretion of pro-inflammatory cytokines, MPO activity, and the protein expression of nuclear factor-κB (NF-κB) in vivo. Moreover, pre-treatment with AS-IV significantly increased the expression levels of manganese superoxide dismutase and cuprum/zinc superoxide dismutase. In the in vitro experiment, treatment of the cells with AS-IV aslo reduced rat pancreatic acinar cell necrosis and nuclear NF-κB activity, and enhanced the protein expression of superoxide dismutase. In conclusion, this study indicates that the protective effects of AS-IV on experimental AP in rats may be closely related to the inhibition of NF-κB. In addition, our results indicate that AS-IV may exert potential antioxidant effects on AP. Therefore, AS-IV may be an effective therapeutic agent for AP.

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Astragaloside IV attenuates Toll-like receptor 4 expression via NF-κB pathway under high glucose condition in mesenchymal stem cells

Cited by 36 publications

References 30 publications

Hyperglycemia magnifies bupivacaine‐induced cell apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress

Hyperglycemia magnifies bupivacaine‐induced cell apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress

Inhibition of RANKL-induced osteoclastogenesis through the suppression of the ERK signaling pathway by astragaloside IV and attenuation of titanium-particle-induced osteolysis

Astragaloside IV ameliorates acute pancreatitis in rats by inhibiting the activation of nuclear factor-κB

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