Tetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-κB pathway

Yang, Xue; Wang, Ying; Feng, Dechun; Xiao, Bao‐Guo; Xu, Lu

doi:10.1111/j.1745-7254.2008.00734.x

Cited by 46 publications

(35 citation statements)

References 35 publications

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“…For this reason, extensive efforts have been made to develop new treatments targeting NF-κB. Tetrandrine, a traditional Chinese herb, has been recently demonstrated to be a potent inhibitor of NF-κB activation and can inhibit effectively the expression of proinflammatory cytokine [31,37,38]. Further studies have demonstrated that the inhibitory effect of tetrandrine on NF-κB activation can be attributed to its ability to prevent the degradation of IκBα, a cytoplasmic inhibitor of the NF-κB and inhibit nuclear translocation of p65 by blocking IκBα kinases α and β activities [28,29].…”

Section: Discussionmentioning

confidence: 99%

Tetrandrine suppresses amyloid-β-induced inflammatory cytokines by inhibiting NF-κB pathway in murine BV2 microglial cells

Qiu

et al. 2011

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Tetrandrine suppresses amyloid-β-induced inflammatory cytokines by inhibiting NF-κB pathway in murine BV2 microglial cells

Qiu

et al. 2011

International Immunopharmacology

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“…However, we think ␣ -crystallin and LPS may have different effects on specific pathways that compete with each other in activating the microglia. NF-B is well known for playing an important role in LPSinduced microglial activation and proinflammation release [31] . However, crystalline can inhibit NF-B-mediated release of inflammatory factors under inflammatory conditions and may be an efficacious therapy in autoimmune demyelination [13] .…”

Section: Discussionmentioning

confidence: 99%

α-Crystallin Downregulates the Expression of TNF-α and iNOS by Activated Rat Retinal Microglia in vitro and in vivo

Wang

Zhao

et al. 2009

Ophthalmic Res

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Purpose: Inhibition of microglial activation has become an important strategy to attenuate neurotoxic damage to the central nervous system. We evaluated the effects of α-crystallin on the production of cytokines in lipopolysaccharides (LPS) and optic nerve injury-activated retinal microglia. Methods: Microglia were collected from retinas of newborn rats, cultured and treated with LPS in vitro. Microglia were also activated by an optic nerve crush in vivo. Pretreatments with and without α-crystallin were performed in cultured cells, and by intravitreal injection in adult rats. Expression of tumor necrosis factor-α (TNF-α), nitric oxide (NO) and inducible NOS synthase (iNOS) were measured by RT-PCR, ELISA, Western blot and the nitrate reductase method. Results: Activated microglia significantly upregulated TNF-α and iNOS mRNA expression and protein production in vitro. An optic nerve crush also increased expression of retinal iNOS and TNF-α protein. Treatment with α-crystallin in vitro and in vivo downregulated their expression. Conclusion: The protective effect of α-crystallin may be due to its effect on microglia via a downregulation in the expression and release of 2 key immune regulatory and inflammatory molecules: TNF-α and iNOS.

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“…Microglia were isolated from primary cultures of rat brains as previously described (Xue et al 2008). Briefly, after brains were dissected and the meninges were carefully stripped, brains were triturated using a blue-tip-mount pipette.…”

Section: Microglia Culture and Drugs Treatmentmentioning

confidence: 99%

Differential Roles of PKA and Epac on the Production of Cytokines in the Endotoxin-Stimulated Primary Cultured Microglia

et al. 2010

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To further understand the anti-inflammatory effect of adenosine cyclic 3',5'-monophosphate (cAMP), we examined the effect of protein kinase A (PKA) and cAMP-responsive guanine nucleotide exchange factor (Epac) on the transcription and production of cytokines and on the activity of mitogen-activated protein kinases (MAPK) p38 and glycogen synthase kinase-3β (GSK-3β) in endotoxin-treated rat primary cultured microglia. The PKA specific agonist N6-benzoyladenosine-3,5-cAMP (6-Bnz-cAMP) not only inhibited the transcription and production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) but also enhanced the transcription and expression of IL-10, while the Epac selective analog 8-(4-chlorophenylthio)-2-O-methyladenosine-3,5-cAMP (8-pCPT-2'-O-Me-cAMP) merely repressed the TNF-α expression. Western blots assays indicated that 6-Bnz-cAMP significantly inhibited lipopolysaccharide-induced activation of both p38 and GSK-3β in a dose-dependent manner; in contrast, 8-pCPT-2'-O-Me-cAMP only slightly repressed GSK-3β activity at large doses. Pretreatment with H-89, a specific PKA antagonist, could completely reverse the effect of 6-Bnz-cAMP on cytokines expressions and kinases activities but had no effect on the performance of 8-pCPT-2'-O-Me-cAMP. Our findings indicate that PKA and Epac exert differential effect on the expression of inflammatory cytokines such as TNF-α, IL-1β, and IL-10, possibly owing to the different effects on the downstream effectors, MAPK p38, and GSK-3β.

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Tetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-κB pathway

Cited by 46 publications

References 35 publications

Tetrandrine suppresses amyloid-β-induced inflammatory cytokines by inhibiting NF-κB pathway in murine BV2 microglial cells

Tetrandrine suppresses amyloid-β-induced inflammatory cytokines by inhibiting NF-κB pathway in murine BV2 microglial cells

α-Crystallin Downregulates the Expression of TNF-α and iNOS by Activated Rat Retinal Microglia in vitro and in vivo

Differential Roles of PKA and Epac on the Production of Cytokines in the Endotoxin-Stimulated Primary Cultured Microglia

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