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

He, Fu Qian; Qiu, Bo; Li, Tian Ke; Xie, Quan; Cui, De Jun; Huang, Xiao Li; Gan, Hua

doi:10.1016/j.intimp.2011.03.023

Cited by 46 publications

(41 citation statements)

References 35 publications

(50 reference statements)

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“…Several studies have indicated that IL-1, IL-6, IL-1β, tumor necrosis factor-α (TNF-α), MIP-1α, and MCP-1 dramatically increase after incubating cultured microglia cells with Aβ [27][28][29][30][31]. These results demonstrate that Aβ can promote the expression of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 78%

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

Liu¹,

Liu

Cao

et al. 2011

Inflammation

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Age-related macular degeneration (AMD) is the predominant cause of irreversible blindness in the elderly population. Despite intensive basic and clinical research, its pathogenesis remains unclear. However, evidence suggests that immunological and inflammatory factors contribute to the pathogenesis of AMD. A newly identified cytokine, IL-33, appears to be an important pro-inflammatory cytokine promoting tissue inflammation. In this study, IL-33 was increased through amyloid-beta(1-40) (Aβ(1-40)) stimulation and regulated inflammatory cytokines including IL-6, IL-8, IL-1β, and TNF-α secretion using different signaling pathways in retinal pigment epithelium (RPE) cells. Furthermore, ST2L, the important component of the IL-33 receptor, was significantly increased following recombinant human IL-33 stimulation in RPE cells. These findings suggest that IL-33-mediated inflammatory responses in RPE cells are involved in the pathogenesis of AMD. Greater understanding of the inflammatory effect of IL-33 and its role in RPE cells should aid the development of future clinical therapeutics and enable novel pharmacological approaches towards the prevention of AMD.

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Section: Discussionmentioning

confidence: 78%

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

Liu¹,

Liu

Cao

et al. 2011

Inflammation

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“…On the other hand, nandrolone decanoate enhanced the deposition of eosinophilic plaques and increased brain susceptibility to beta amyloid fragments (Caraci et al, 2011). Aggregation of the latter fragments may induce reactive oxygen species, inflammatory cytokines, apoptosis, and neuronal mitochondrial dysfunction (Tiffany et al, 2001;He et al, 2011).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Lipoic acid and pentoxifylline mitigate nandrolone decanoate-induced neurobehavioral perturbations in rats via re-balance of brain neurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation of TNFR1 expression

Ahmed

Awdan

2015

Hormones and Behavior

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“…Tetrandrine (Tet, Figure 1) is a compound extracted from the root of Stephania tetrandra and is often used for the treatment of rheumatism, inflammation, occlusive cardiovascular disorders and tumors [1][2][3][4][5][6][7][8] . Some early studies demonstrated that tetrandrine causes hepatotoxicity [9,10] .…”

Section: Introductionmentioning

confidence: 99%

ROS generated by CYP450, especially CYP2E1, mediate mitochondrial dysfunction induced by tetrandrine in rat hepatocytes

Miao

Cai

et al. 2013

Acta Pharmacol Sin

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Aim: Tetrandrine, an alkaloid with a remarkable pharmacological profile, induces oxidative stress and mitochondrial dysfunction in hepatocytes; however, mitochondria are not the direct target of tetrandrine, which prompts us to elucidate the role of oxidative stress in tetrandrine-induced mitochondrial dysfunction and the sources of oxidative stress. Methods: Rat primary hepatocytes were isolated by two-step collagenase perfusion. Mitochondrial function was evaluated by analyzing ATP content, mitochondrial membrane potential (MMP) and the mitochondrial permeability transition. The oxidative stress was evaluated by examining changes in the levels of reactive oxygen species (ROS) and glutathione (GSH). Results: ROS scavengers largely attenuated the cytotoxicity induced by tetrandrine in rat hepatocytes, indicating the important role of ROS in the hepatotoxicity of tetrandrine. Of the multiple ROS inhibitors that were tested, only inhibitors of CYP450 (SKF-525A and others) reduced the ROS levels and ameliorated the depletion of GSH. Mitochondrial function assays showed that the mitochondrial permeability transition (MPT) induced by tetrandrine was inhibited by SKF-525A and vitamin C (VC), both of which also rescued the depletion of ATP levels and the mitochondrial membrane potential. Upon inhibiting specific CYP450 isoforms, we observed that the inhibitors of CYP2D, CYP2C, and CYP2E1 attenuated the ATP depletion that occurred following tetrandrine exposure, whereas the inhibitors of CYP2D and CYP2E1 reduced the ROS induced by tetrandrine. Overexpression of CYP2E1 enhanced the tetrandrineinduced cytotoxicity. Conclusion: We demonstrated that CYP450 plays an important role in the mitochondrial dysfunction induced by the administration of tetrandrine. ROS generated by CYP450, especially CYP2E1, may contribute to the mitochondrial dysfunction induced by tetrandrine.

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

Cited by 46 publications

References 35 publications

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

Lipoic acid and pentoxifylline mitigate nandrolone decanoate-induced neurobehavioral perturbations in rats via re-balance of brain neurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation of TNFR1 expression

ROS generated by CYP450, especially CYP2E1, mediate mitochondrial dysfunction induced by tetrandrine in rat hepatocytes

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