Cardamonin from Alpinia rafflesiana inhibits inflammatory responses in IFN-γ/LPS-stimulated BV2 microglia via NF-κB signalling pathway

Chow, Yuh-Lit; Lee, Ka-Heng; Vidyadaran, Sharmili; Lajis, Nordin H.; Akhtar, M.N.; Israf, Daud Ahmad; Ahmad, Sadeem

doi:10.1016/j.intimp.2012.01.009

Cited by 69 publications

(43 citation statements)

References 33 publications

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“…Apart from this toxin-induced microglial activation, various other triggers involved in microglial activation include immunological insults such as IFN- γ , lipopolysaccharide (LPS), chemokines (CCL5, CCL2, and CXCL10), neurotransmitters, gangliosides, the CD40 ligand, proteases such as thrombin [40], tissue plasminogen activator [41], matrix metalloproteinase-3 (MMP-3) [21], endogenous disease proteins, and neuronal injury itself [42]. Among these activators, LPS-induced neuroinflammation is one of the most accepted and widely used endotoxin models that induces a strong neuroinflammatory response in BV-2 microglial cells [43, 44] or when injected directly into the vicinity of the SN [45]. Recent findings demonstrate that neurons are not simply passive targets of microglia but rather control microglial activation [3, 46, 47].…”

Section: Mediators Of Neuroinflammationmentioning

confidence: 99%

Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease

Kumar

Kim

et al. 2013

Mediators of Inflammation

215

147

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Neuroinflammation is a host-defense mechanism associated with restoration of normal structure and function of the brain and neutralization of an insult. Increasing neuropathological and biochemical evidence from the brains of individuals with Parkinson's disease (PD) provides strong evidence for activation of neuroinflammatory pathways. Microglia, the resident innate immune cells, may play a major role in the inflammatory process of the diseased brain of patients with PD. Although microglia forms the first line of defense for the neural parenchyma, uncontrolled activation of microglia may directly affect neurons by releasing various molecular mediators such as inflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-6, and IL-1β), nitric oxide, prostaglandin E2, and reactive oxygen and nitrogen species. Moreover, recent studies have reported that activated microglia phagocytose not only damaged cell debris but also intact neighboring cells. This phenomenon further supports their active participation in self-enduring neuronal damage cycles. As the relationship between PD and neuroinflammation is being studied, there is a realization that both cellular and molecular mediators are most likely assisting pathological processes leading to disease progression. Here, we discuss mediators of neuroinflammation, which are known activators released from damaged parenchyma of the brain and result in neuronal degeneration in patients with PD.

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Section: Mediators Of Neuroinflammationmentioning

confidence: 99%

Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease

Kumar

Kim

et al. 2013

Mediators of Inflammation

215

147

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“…Recent studies revealed that cardamonin not only possesses anti-inflammation activity, but also suppresses the proliferation of human tumor cells, including myeloma and colorectal carcinoma [16][17][18][19]. However, the mechanism underlying the inhibition effects of cardamonin on the cancer cells is not well documented, although inhibition of mTOR, Tgase-2, and NF-kB may be associated with its bioactivity [20][21][22]. In the present study, we investigated the effects of cardamonin on the self-renewal and cell apoptosis in GSCs and its association with STAT3 pathway.…”

Section: Introductionmentioning

confidence: 99%

Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

Liu

Zhao

et al. 2015

Tumor Biol.

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Glioblastoma stem cells (GSCs) are the initiating cells in glioblastoma multiforme (GBM) and contribute to the resistance of GBM to chemotherapy and radiation. In the present study, we investigated the effects of cardamonin (3,4,2,4-tetrahydroxychalcone) on the self-renewal and apoptosis of GSCs, and if its action is associated with signal transducer and activator of transcription 3 (STAT3) pathway. CD133(+) GSCs, a kind of GSCs line, was established from human glioblastoma tissues. Cardamonin inhibited the proliferation and induced apoptosis in CD133+ GSCs. The proapoptotic effects of temozolomide (TMZ) were further enhanced by cardamonin in CD133+ GSCs and U87 cells in vitro. For in vivo study, injection of 5 × 10(5) cells of CD133+ GSCs subcutaneously (s.c.) into nude mice, 100 % of large tumors were developed within 8 weeks in all mice; in contrast, only one out of five mice developed a small tumor when 5 × 10(5) cells of CD133(-) GMBs cells were injected. Cardamonin also inhibited STAT3 activation by luciferase assay and suppressed the expression of the downstream genes of STAT3, such as Bcl-XL, Bcl-2, Mcl-1, survivin, and VEGF. Furthermore, cardamonin locked nuclear translocation and dimerization of STAT3 in CD133(+) GSCs. Docking analysis confirmed that cardamonin molecule was successfully docked into the active sites of STAT3 with a highly favorable binding energy of -10.78 kcal/mol. The study provides evidence that cardamonin is a novel inhibitor of STAT3 and has the potential to be developed as a new anticancer agent targeting GSCs. This study also reveals that targeting STAT3 signal pathway is an important strategy for the treatment of human GBM.

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“…These research results suggest that the reason telmisartan and Tek-1 reduced glial cell inflammatory response is related to activation of PPAR gamma and inhibition of NF-κb signal pathway. Tek-1 exerts a more obvious effect than telmisartan in inhibiting NF-κb signal pathway [14]. …”

Section: Discussionmentioning

confidence: 99%

The pharmacological research of Tek-1 relevance to anti-neuroinflammation, a candidate compound based on Telmisartan

Yang

Cui

2015

Open Medicine

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In this paper, BV-2 mouse small glial cell inflammation model induced by LPS is established. The experiment used 0.1–10 μM of telmisartan and Tek-1 to incubate with small glial cell and used telmisartan and Tek-1 to incubate with PPAR gamma special heterosexual antagonistic anti-agent GW9662. The article used ELISA method to dectect TNF-a effect on small glial cell for telmisartan and Tek-1. The article used real-time quantitative PCR method to dectect mRNA level expression effect of CD11b, CD16 and iNOS on small glial cell for telmisartan and Tek-1 and used Western Blot method to dectect MAPKs signal pathway and NF-κb signal turned guide pathway effect on small glial cell for telmisartan and Tek-1. Results show that Tek-1 had high affinity with AT1 receptor and inhibited intracellular calcium ion activation which can be for the AT1 receptor antagonists. Meanwhile, Tek-1 can partially activate PPAR gamma compared with full agonists of rosiglitazone.

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Cardamonin from Alpinia rafflesiana inhibits inflammatory responses in IFN-γ/LPS-stimulated BV2 microglia via NF-κB signalling pathway

Cited by 69 publications

References 33 publications

Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease

Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease

Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

The pharmacological research of Tek-1 relevance to anti-neuroinflammation, a candidate compound based on Telmisartan

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