scholarly journals Selenium ameliorates S. aureus-induced inflammation through ROS-mediated NLRP3 inflammasome in bovine mammary epithelial cells

2020 ◽  
Author(s):  
Chongliang Bi ◽  
Shujiu Zhang ◽  
He Tang ◽  
Hui Li
Keyword(s):  
Protein Expression ◽  
Nlrp3 Inflammasome ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Expression Level ◽  
Bovine Mammary Epithelial Cells ◽  
Caspase 1 ◽  
Through Flow ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Abstract Background Some research has indicated that selenium (Se) plays a significant role during mastitis. However the intracellular anti-inflammatory effect of Se is not fully clear. Due to the ability of Staphylococcus aureus ( S. aureus ) to internalize into host cell, in this study we explored whether Se could regulate inflammation induced by S. aureus through reactive oxygen species (ROS)-mediated NLRP3 inflammasome in bMECs. Result bMECs were treated with 8 μmol/L Na 2 SeO 3 for 12 h before infected with S. aureus for 2 h. Through flow cytometry, Western blot and qPCR analysis, ROS and NLRP3 imflammasome were detected. Result shown that the production of ROS was increased by S. aureus , Se exerted strong inhibitory effects on the production of ROS; The protein expression of NLRP3 inflammasome including NLRP3, ASC and Caspase-1 increased significantly after S. aureus infection, Se played an important role in regulating the expression of NLRP3, ASC and Caspase-1; To further investigate the anti-inflammatory effect of Se, the expression level of IL-1β associated molecule pro-IL-1β and IL-1β were detected. Result shown that the mRNA expression of IL-1β was up-regulated by S. aureus and after Se treatment the expression level of IL-1β mRNA was markedly down-regulated, meanwhile Se play a regulation effect on the protein expression of Pro-IL-1β and IL-1β. Conclusions Here we show that ROS is involved in bMECs inflammation induced by S. aureus and Se ameliorates S. aureus -induced inflammation through ROS-mediated NLRP3 pathway in bMECs.

scholarly journals Sesquiterpenoids and Their Anti-Inflammatory Activity: Evaluation of Ainsliaea yunnanensis

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1701
Author(s):  
Jinjie Li ◽  
Xiuting Li ◽  
Xin Wang ◽  
Xiangjian Zhong ◽  
Linlin Ji ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Ethanolic Extract ◽  
The Self ◽  
Inflammatory Activity ◽  
Spectroscopic Methods ◽  
Activity Evaluation ◽  
Caspase 1 ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Four new sesquiterpenoids (1–4) and six known sesquiterpenoids (5–10), were isolated from the EtOAc phase of the ethanolic extract of Ainsliaea yunnanensis. Their structures were established by spectroscopic methods, including 1-D, 2-D NMR and HPLC-MS. All compounds were tested for their anti-inflammatory effect by the inhibition of the activity of NLRP3 inflammasome by blocking the self-slicing of pro-caspase-1, which is induced by nigericin, then the secretion of mature IL-1β, mediated by caspase-1, was suppressed. Unfortunately none of the compounds showed an anti-inflammatory effect.

Antioxidant and anti-inflammatory effects of pomegranate peel extracts on bovine mammary epithelial cells BME-UV1

2018 ◽  
Vol 34 (10) ◽  
pp. 1465-1469 ◽  
Author(s):  
Fabio Mastrogiovanni ◽  
Roberta Bernini ◽  
Loredana Basiricò ◽  
Umberto Bernabucci ◽  
Margherita Campo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Pomegranate Peel ◽  
Bovine Mammary Epithelial Cells ◽  
Anti Inflammatory

scholarly journals 3β,23-Dihydroxy-12-ene-28-ursolic Acid Isolated from Cyclocarya paliurus Alleviates NLRP3 Inflammasome-Mediated Gout via PI3K-AKT-mTOR-Dependent Autophagy

2022 ◽  
Vol 2022 ◽  
pp. 1-15
Author(s):  
Dongxiao Lou ◽  
Xiaogai Zhang ◽  
Cuihua Jiang ◽  
Fang Zhang ◽  
Chao Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Ursolic Acid ◽  
Nlrp3 Inflammasome ◽  
Soft Tissues ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Expression Level ◽  
Expression Ratio ◽  
Cyclocarya Paliurus ◽  
Caspase 1

Gout is regarded as a painful inflammatory arthritis induced by the deposition of monosodium urate crystals in joints and soft tissues. Nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated IL-1β production plays a crucial role in the pathological process of gout. Cyclocarya paliurus (CP) tea was found to have an effect on reducing the blood uric acid level of people with hyperuricemia and gout. However, its medicinal ingredients and mechanism for the treatment of gout are still unclear. Thus, this study was designed to investigate the effects of the active triterpenoids isolated from C. paliurus on gout and explore the underlying mechanism. The results showed that compound 2 (3β,23-dihydroxy-12-ene-28-ursolic acid) from C. paliurus significantly decreased the protein expression of IL-1β, caspase-1, pro-IL-1β, pro-caspase-1, and NLRP3. Furthermore, the production of ROS in the intracellular was reduced after compound 2 treatment. However, ROS agonist rotenone remarkably reversed the inhibitory effect of compound 2 on the protein expression of NLRP3 inflammasome. Additionally, the expression level of LC3 and the ratio of LC3II/LC3I were increased, but the expression level of p62 was suppressed by compound 2 whereas an autophagy inhibitor 3-methyladenine (3-MA) significantly abolished the inhibitory effects of compound 2 on the generation of ROS and the protein expression of NLRP3 inflammasome. Moreover, compound 2 could ameliorate the expression ratio of p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR. Interestingly, mTOR activator MHY-1485 could block the promotion effect of compound 2 on autophagy regulation and inhibitory effect of compound 2 on induction of ROS and IL-1β. In conclusion, these findings suggested that compound 2 may effectively improve NLRP3 inflammasome-mediated gout via PI3K-AKT-mTOR-dependent autophagy and could be further investigated as a potential agent against gout.

scholarly journals PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Qing-Qi Meng ◽  
Zhen-Cheng Feng ◽  
Xing-Liang Zhang ◽  
Li-Qiong Hu ◽  
Min Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Functional Recovery ◽  
Nlrp3 Inflammasome ◽  
Interleukin 1 ◽  
Peroxisome Proliferator ◽  
Caspase 1 ◽  
Cord Injury ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Persistent inflammation disrupts functional recovery after spinal cord injury (SCI). Peroxisome proliferator-activated receptor gamma (PPAR-γ) activation promotes functional recovery in SCI rats by inhibiting inflammatory cascades and increasing neuronal survival. We sought to clarify the relationship between PPAR-γ activation and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome suppression, and the role of NF-κB in activating the NLRP3 inflammasome in neurons. In SCI rats, we found that rosiglitazone (PPAR-γ agonist) inhibited the expression of caspase-1. In in vitro neurons, G3335 (PPAR-γ antagonist) reversed the rosiglitazone-induced inhibition of caspase-1, interleukin 1 (IL-1β), and interleukin 6 (IL-6). Rosiglitazone inhibited the expression of NLRP3, caspase-1, IL-1β, and IL-6. However, the activator of NLRP3 could counteract this inhibition induced by PPAR-γ activation. NF-κB did not participate in the process of rosiglitazone-induced inhibition of NLRP3. Consistent with our in vitro results, we verified that locomotor recovery of SCI rats in vivo was regulated via PPAR-γ, NLRP3, and NF-κB. These results suggest that PPAR-γ activation exerts an anti-inflammatory effect by suppressing the NLRP3 inflammasome—but not NF-κB—in neurons and that PPAR-γ activation is a promising therapeutic target for SCI.

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