scholarly journals HMGB1-Binding Heptamer Confers Anti-Inflammatory Effects in Primary Microglia Culture

2013 ◽  
Vol 22 (4) ◽  
pp. 301-307 ◽  
Author(s):  
Il-Doo Kim ◽  
Ja-Kyeong Lee
Keyword(s):  
Primary Microglia ◽  
Anti Inflammatory

scholarly journals Platycodigenin as Potential Drug Candidate for Alzheimer’s Disease via Modulating Microglial Polarization and Neurite Regeneration

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3207 ◽  
Author(s):  
Zhiyou Yang ◽  
Baiping Liu ◽  
Long-en Yang ◽  
Cai Zhang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Neurons ◽  
Neuronal Survival ◽  
Critical Role ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factors ◽  
Primary Microglia ◽  
Microglial Polarization ◽  
Anti Inflammatory

Neuroinflammatory microenvironment, regulating neurite regrowth and neuronal survival, plays a critical role in Alzheimer’s disease (AD). During neuroinflammation, microglia are activated, inducing the release of inflammatory or anti-inflammatory factors depending on their polarization into classical M1 microglia or alternative M2 phenotype. Therefore, optimizing brain microenvironment by small molecule-targeted microglia polarization and promoting neurite regeneration might be a potential therapeutic strategy for AD. In this study, we found platycodigenin, a naturally occurring triterpenoid, promoted M2 polarization and inhibited M1 polarization in lipopolysaccharide (LPS)-stimulated BV2 and primary microglia. Platycodigenin downregulated pro-inflammatory molecules such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6 and nitric oxide (NO), while upregulated anti-inflammatory cytokine IL-10. Further investigation confirmed that platycodigenin inhibited cyclooxygenase-2 (Cox2) positive M1 but increased Ym1/2 positive M2 microglial polarization in primary microglia. In addition, platycodigenin significantly decreased LPS-induced the hyperphosphorylation of mitogen-activated protein kinase (MAPK) p38 and nuclear factor-κB (NF-κB) p65 subunits. Furthermore, the inactivation of peroxisome proliferators-activated receptor γ (PPARγ) induced by LPS was completely ameliorated by platycodigenin. Platycodigenin also promoted neurite regeneration and neuronal survival after Aβ treatment in primary cortical neurons. Taken together, our study for the first time clarified that platycodigenin effectively ameliorated LPS-induced inflammation and Aβ-induced neurite atrophy and neuronal death.

Neuroprotective effect of Lithospermum officinale callus extract on inflamed primary microglial cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Maryam Kheyrollah ◽  
Farzaneh Sabouni ◽  
Mohsen Farhadpour ◽  
Kamahldin Haghbeen
Keyword(s):  
Neuroprotective Effect ◽  
Wistar Rat ◽  
Microglial Cells ◽  
Root Extract ◽  
Primary Microglia ◽  
Methanolic Extracts ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Anti Inflammatory ◽  
Lithospermum Officinale

Background and Objective: Lithospermum officinale is a famous medicinal herb in the traditional medicine of India. However, the medicinal use of its root extract is limited due to the presence of pyrrolizidine alkaloids (PzAl). It was recently shown that PzAl are not accumulated in the cell culture of L. officinale while the biosynthetic pathway of phenolic acids remains active so that rosmarinic acid (RsA) is the main product in the proliferated callus. Considering the existing literature on the anti-inflammatory effects of caffeic acid (CfA) and its derivatives, this research was devoted to the evaluation of the anti-inflammatory capacity of methanolic extracts of L. officinale callus (LoE) on the rat microglial cells as the immune cells of the Central Nervous System, which play an essential role in the responses to neuroinflammation. Methods: primary microglia were obtained from Wistar rat, then they were subjected to various amounts of CfA and methanolic extracts of 17 and 31-day L. officinale callus prior to stimulation by LPS. In addition to HPLC analysis of the extracts, viability, nitric oxide production, evaluation of the pro-inflammatory genes and cytokines in the inflamed microglia were investigated. Results: Methanolic extract of the 17-day old callus of L. officinale exhibited anti-inflammatory effects on the LPS- stimulated microglial cells much higher than that was observed for CfA. The data was further supported by the decreased expression of NOS2, TNF-α, and Cox-2 mRNA and the suppression of TNF-α and IL-1β release in the activated microglial cells pretreated with the effective dose of LoE (0.8 mg mL-1). Conclusion: It was assumed that better anti-neuroinflammatory performance of LoE than CfA in LPS-activated primary microglia could be a result of synergism of the components of the extract and the lipophilic nature of RsA as the main phenolic acid of LoE. Considering the fact that LoE shows high antioxidant capacity and lacks PzAl, it is anticipated that LoE is considered as a reliable substitute to the extract of the natural root of L. officinale and plays a key role in the preparation of neuroprotective pharmaceutical formula.

scholarly journals Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

2020 ◽  
Author(s):  
Jinqiang Zhang ◽  
Saini Yi ◽  
Chenghong Xiao ◽  
Yahui Li ◽  
Chan Liu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Neurological Diseases ◽  
Pathological Process ◽  
Dependent Manner ◽  
Primary Microglia ◽  
Neuronal Function ◽  
Ppar Γ ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Different Doses

AbstractMicroglia cells are the main mediators of neuroinflammation. Activation of microglia often aggravates the pathological process of various neurological diseases. Natural chemicals have unique advantages in inhibiting microglia-mediated neuroinflammation and improving neuronal function. Here, we examined the effects of asperosaponin VI (ASA VI) on LPS-activated primary microglia. Microglia were isolated from mice and pretreated with different doses of ASA VI, following lipopolysaccharide (LPS) administration. Activation and inflammatory response of microglia cells were evaluated by q-PCR, immunohistochemistry and ELISA. Signaling pathways were detected by western blotting. We found that the ASA VI inhibited the morphological expansion of microglia cells, decreased the expression and release of proinflammatory cytokines, and promoted the expression of antiinflammatory cytokines in a dose-dependent manner. ASA VI also activated PPAR-γ signaling pathway in LPS-treated microglia. The anti-inflammatory effects of ASA VI in microglia were blocked by treating PPAR-γ antagonist (GW9662). These results showed that ASA VI promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-γ pathway.

Anti-inflammatory properties of Honokiol in activated primary microglia and astrocytes

2018 ◽  
Vol 323 ◽  
pp. 78-86 ◽  
Author(s):  
Uta Rickert ◽  
François Cossais ◽  
Marvin Heimke ◽  
Philipp Arnold ◽  
Andrea Preuße-Prange ◽  
...  
Keyword(s):  
Primary Microglia ◽  
Anti Inflammatory

scholarly journals CQMUH-011 Inhibits LPS-Induced Microglia Activation and Ameliorates Brain Ischemic Injury in Mice

Inflammation ◽  
2021 ◽  
Author(s):  
Hailin Liu ◽  
Xiangnan Hu ◽  
Rong Jiang ◽  
Jianghui Cai ◽  
Qiao Lin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cerebral Ischemia ◽  
Microglial Activation ◽  
Ischemia Reperfusion ◽  
Nuclear Antigen ◽  
Primary Microglia ◽  
Activated Microglia ◽  
Acute Cerebral Ischemia ◽  
Anti Inflammatory

Abstract Excessive microglial activation-mediated neuroinflammation is closely involved in the pathogenesis of several neurological diseases. CQMUH-011, as a novel adamantane sulfonamide compound, has been shown anti-inflammatory properties in activated macrophages (RAW264.7). However, the role of CQMUH-011 in microglial activation-induced neuroinflammation and neuroprotective properties has yet to be elucidated. In the present study, we investigated the potential effects and mechanisms of CQMUH-011 on lipopolysaccharide (LPS)-stimulated primary microglia in vitro and transient middle cerebral artery occlusion (t-MCAO)–induced acute cerebral ischemia/reperfusion (I/R) injury in vivo. The results demonstrated that CQMUH-011 significantly suppressed the production of tumor necrosis factor (TNF)-α and interleukin (IL)-1β by LPS-stimulated primary microglia. In addition, CQMUH-011 inhibited the proliferation of activated microglia by arresting the cell cycle at the G1/S phase accompanied by downregulating the expression of cell cycle regulatory proteins such as proliferating cell nuclear antigen (PCNA) and cyclin D1. CQMUH-011 was seen to induce apoptosis in activated microglia by regulating the expression of Bax and Bcl-2. Furthermore, CQMUH-011 markedly attenuated the protein expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) as well as the phosphorylation levels of nuclear factor-kappa (NF-κB) subunit p65, inhibitory kappa B-alpha (IκBα), and mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase (ERK) and p38 kinases. In vivo, CQMUH-011 administration significantly improved neurological function and infarct volume, and ameliorated the inflammatory cytokines and microglia amount around the injury site of mice. In conclusion, these results suggested that CQMUH-011 has a notable anti-inflammatory effect and protects mice from I/R injure. Thus, CQMUH-011 may be a candidate drug for the treatment of cerebral ischemia patients.

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