<i>Lonicera japonica</i>THUNB. Extract Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses by Suppressing NF-<i>κ</i>B Signaling in BV-2 Microglial Cells

Kwon, Seung-Hwan; Ma, Shi-Xun; Hong, Sa-Ik; Lee, Seok‐Yong; Jang, Choon‐Gon

doi:10.1089/jmf.2014.3341

Cited by 27 publications

(12 citation statements)

References 67 publications

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“…For in vitro studies, the mouse microglial BV‐2 cell line was obtained from Professor Choon‐gon Jang of the School of Pharmacy at Sungkyunkwan University . BV2 cells were cultured in Dulbecco's modified Eagle's medium (Gibco) containing 10% heat‐inactivated fetal bovine serum (30‐2020, ATCC) and antibiotics (100 μg/mL streptomycin and 100 IU/mL penicillin, Gibco).…”

Section: Methodsmentioning

confidence: 99%

Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Lee

Kim

et al. 2018

CNS Neurosci Ther

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Section: Methodsmentioning

confidence: 99%

Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Lee

Kim

et al. 2018

CNS Neurosci Ther

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“…LPS activates innate immune cells, which leads to the production of pro-inflammatory cytokines (22). It has been reported that citrate is able to modulate LPS-induced monocyte inflammatory responses (23) and that suppression of NF-κB signaling in BV-2 microglial cells inhibits LPS-induced inflammatory responses (24). The present study demonstrated that LPS treatment significantly increased the release of inflammatory cytokines TNF-α and IL-1β, which indicated that LPS was able to induce the inflammatory response in NK92 cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of granzyme B activity blocks inflammation induced by lipopolysaccharide through regulation of endoplasmic reticulum stress signaling in NK92 cells

et al. 2018

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Granzyme B (GrB) is a serine protease that is expressed in the lytic granules of natural killer (NK) cells and cytotoxic T lymphocytes (CTL), and which has been widely reported to serve a crucial role for target cell apoptosis. GrB may serve a non‑cytotoxic role in inflammation, but the evidence remains unclear. The present study aimed to establish an inflammatory cell model by using NK92 cells stimulated with lipopolysaccharide (LPS) to investigate whether GrB was involved in the development of inflammation. The extracellular levels of tumor necrosis factor‑α (TNF‑α), interleukin‑1β (IL‑1β) and GrB were examined by ELISA, and it was demonstrated that LPS treatment increased the extracellular levels of TNF‑α, IL‑1β and GrB, and these increased expression levels were inhibited by pretreatment with the GrB inhibitor serpin A3N (SA3N). The protein expression levels of glucose‑regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), nuclear factor‑κB (NF‑κB), inhibitor of NF‑κB (IκBα) and GrB were examined by western blot analysis. The results demonstrated that LPS stimulation increased the expression levels of GRP78, CHOP, NF‑κB and GrB, and decreased the expression of IκBα, and these changes were inhibited by SA3N, which indicated that inhibition of GrB activity may suppress endoplasmic reticulum (ER) stress signaling. Therefore, it was suggested that GrB may be a potential pro‑inflammatory factor, and inhibition of GrB activity may aid the prevention of the development of inflammation by suppressing ER stress signaling.

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“…The mouse microglial cell line, BV-2, was kindly provided by Prof. Choon-gon Jang at Sungkyunkwan University [ 49 ]. The rat glioma cell line (C6) was obtained from American Type Culture Collection (Manassas, Virginia, USA).…”

Section: Methodsmentioning

confidence: 99%

Streptococcus pneumoniae induces pyroptosis through the regulation of autophagy in murine microglia

et al. 2015

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Streptococcus pneumoniae is responsible for significant mortality and morbidity worldwide and causes invasive pneumococcal diseases including pneumococcal meningitis. Pyroptosis is caspase-1-dependent inflammatory cell death and is known to be induced by various microbial infections. In the present study, we investigated the molecular mechanisms that regulate pyroptosis induced by S. pneumoniae in microglia. Our results revealed that S. pneumoniae induced pyroptosis through caspase-1 activation and IL-1β production. We also found that the activation of caspase-1 and the maturation of IL-1β and IL-18 in the S. pneumoniae-triggered pyroptotic cell death process were mediated by NLRP3 inflammasome. In addition, pneumococcal infection increased the expression of autophagy-related genes and induced autophagosome formation. We also showed that the inhibition of autophagy promoted pneumococcus-induced pyroptosis. Furthermore, ROS was generated by pneumococcal infection and inhibited caspase-1 activation within 4 h of infection. However, in the late phase of infection, IL-1β secretion and caspase-1-dependent cell death were induced by ROS. These results suggest that autophagy induction transiently delay pyroptosis induced by S. pneumoniae in microglia. Our study also revealed that the activation of caspase-1 and the production of IL-1β were induced by pneumolysin and that pneumolysin triggered pyroptosis in microglial cells. Similar to the in vitro results, S. pneumoniae induced caspase-1 activation and caspase-1-dependent cytokine maturation in the mouse meningitis model. Thus, the present data demonstrate that S. pneumoniae induces pyroptosis in murine microglia and that NLRP3 inflammasome is critical for caspase-1 activation during the process. Furthermore, the induction of autophagy could transiently protect microglia from pyroptosis.

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Lonicera japonicaTHUNB. Extract Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses by Suppressing NF-κB Signaling in BV-2 Microglial Cells

Cited by 27 publications

References 67 publications

Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Inhibition of granzyme B activity blocks inflammation induced by lipopolysaccharide through regulation of endoplasmic reticulum stress signaling in NK92 cells

Streptococcus pneumoniae induces pyroptosis through the regulation of autophagy in murine microglia

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