Toll‐like receptors in the functional orientation of cardiac progenitor cells

Yousefi, Mohammadreza; Mamipour, Mina; Sokullu, Emel; Ghaderi, Shahrooz; Amini, Hassan; Rahbarghazi‬, Reza

doi:10.1002/jcp.28738

Cited by 1 publication

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“…12,32,33 TLR4, one of the most important types of TLR families, is a transmembrane glycoprotein that plays a key role in the innate immune system and it is related to the secretion of multiple inflammatory cytokines. 34,35 Briefly, LPS attaches to the TLR4-MD2 complex and triggers the phosphorylation of NFκB, and p-NFκB leads to the upregulation of pro-inflammatory cytokines. In the present study, Aβ-induced BV-2 cells showed up-regulation of ROS, MDA, and pro-inflammatory cytokines, which are consistent with the previous studies.…”

Section: Discussionmentioning

confidence: 99%

<p>Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway</p>

Li¹,

Lv²,

Wu³

et al. 2020

NDT

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Background: β-Amyloid (Aβ) induces oxidative stress and inflammation of microglial cells, thus leading to Alzheimer's disease. Methyl jasmonate (MeJA) is reported to have antiinflammatory and anti-oxidant effects. However, the potential roles of MeJA in Aβ-induced cell activities and the underlying mechanism are unclear. Methods: Microglial cell line BV-2 was stimulated by 20 μM Aβ and/or 20 μM MeJA and then divided into four groups (control, Aβ, MeJA, and Aβ+MeJA). Cell viability was detected by MTT assay. MDA, SOD activity, and ROS were detected by fluorescence spectrophotometry and immunofluorescence assay. Nrf2 and HO-1 were detected by qRT-PCR and Western blot. Furthermore, inflammatory cytokines (p-NFκB, TLR4, TNF-α, IL-1β, and IL-6) and apoptosis factors (Bcl-2, Bax, and cl-casp-3) were detected by Western blot. TUNEL assay was applied to investigate apoptosis rate. Moreover, the mechanism of how MeJA played anti-oxidative stress and anti-inflammatory roles was investigated by silencing of Nrf2 via siRNA. Results: The result of MTT assay showed that MeJA improved the decreased viability of BV-2 cells induced by Aβ. The detection of MDA, SOD activity, and ROS showed the oxidative stress levels were decreased in Aβ+MeJA group compared with Aβ group. Nrf2, HO-1, and SOD were significantly up-regulated in Aβ+MeJA group compared with Aβ group (p<0.01). In contrast, inflammatory cytokines were significantly down-regulated in Aβ +MeJA group compared with Aβ group (p<0.05). Similarly, the expressions of apoptosis cytokines and TUNEL assay suggested a decreased apoptosis rate in Aβ+MeJA group compared to Aβ group (p<0.01). Finally, results of Nrf2 knockdown experiment showed down-regulations of anti-oxidative stress factors (Nrf2, HO-1 and SOD), up-regulations of inflammatory cytokines, and increased ratio of Bax to Bcl in Aβ+MeJA+si-Nrf2 group compared with Aβ+MeJA group (p<0.01). Conclusion: MeJA could relieve Aβ-induced oxidative stress and inflammatory response in microglial cells by activating Nrf2/HO-1 pathway.

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