Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
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Biomed. Pharmacother. · Jan 2019
Farrerol attenuates β-amyloid-induced oxidative stress and inflammation through Nrf2/Keap1 pathway in a microglia cell line.
Farrerol, an important bioactive constituent of rhododendron, exhibits broad activities such as anti-oxidative and anti-inflammatory effects. Recent studies showed that farrerol possesses neuroprotective activity, however, the mechanism has not been reported. The aim of the present study was to investigate the protective effect of farrerol on β-amyloid (Aβ)-induced mouse microglial BV-2 cells and the underlying mechanism. ⋯ Knockdown of Nrf2 by small interfere RNA (siRNA) targeting Nrf2 (si-Nrf2) abolished the protective effect of farrerol on Aβ-induced BV-2 cells. In conclusion, farrerol attenuated Aβ-induced oxidative stress and inflammation in BV-2 cells through enhancing the activation of Nrf2/Keap1 pathway. The findings indicated that farrerol could be considered as a therapeutic approach for the treatment of Alzheimer's disease (AD).
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Biomed. Pharmacother. · Jan 2019
Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions.
Spinal cord injury (SCI) is a devastating event, leading to the progression of chronic neuropathic pain syndrome. Triggering receptor expressed on myeloid cells 1 (TREM1) is an innate immune receptor expressed on neutrophils and monocytes/macrophages. TREM1 enhances inflammatory response in various models of diseases, but its significance in SCI remains unclear. ⋯ Of note, the in vitro results also demonstrated that suppressing HO-1 expressions using Zn-protoporphyrin (ZnPP) abrogated TREM1KD-reduced inflammation, oxidative stress and glial cells activation. The results above demonstrated that suppressing TREM1 expressions markedly improved the outcome of SCI, most likely through reducing inflammation and oxidative stress at least partly regulated by HO-1 expressions. TREM1 inhibition might be therefore has potential as a therapeutic target after SCI.
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Biomed. Pharmacother. · Jan 2019
α, β-Amyrin, a pentacyclic triterpenoid from Protium heptaphyllum suppresses adipocyte differentiation accompanied by down regulation of PPARγ and C/EBPα in 3T3-L1 cells.
Previous studies have reported the anti-obesity effects of α, β-Amyrin in high fat-fed mice. This study aimed to evaluate whether α, β-Amyrin has an anti-adipogenic effect in 3T3-L1 murine adipocytes and to explore the possible underlying mechanisms. 3T3-L1 pre-adipocytes were differentiated in a medium containing insulin, dexamethasone, and 1-methyl-3-isobutylxanthine. Cytotoxicity of α, β-Amyrin was assessed by MTT assay. ⋯ In addition, the protein expression of membrane GLUT4 in 3T3- L1 adipocytes treated with α, β-Amyrin was significantly higher than in control cells, indicating that α, β-Amyrin augments glucose uptake. These findings suggest that α, β-Amyrin exerts an anti-adipogenic effect principally via modulation of lipid and carbohydrate metabolism in 3T3-L1cells. The present in vitro findings, taken together with our earlier observation of the anti-obesity effect in vivo, suggest that α, β-Amyrin can be developed as a new therapeutic agent for treatment and prevention of obesity.
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Biomed. Pharmacother. · Jan 2019
Long noncoding RNA RMRP upregulation aggravates myocardial ischemia-reperfusion injury by sponging miR-206 to target ATG3 expression.
Coronary heart disease is a common cause of death and disability worldwide and mainly results from myocardial ischemia-reperfusion (I/R) injury. This study aimed to elucidate the roles and possible mechanism of long noncoding RNA Component Of Mitochondrial RNA Processing Endoribonuclease (RMRP) in protecting against ischemic myocardial injury. ⋯ Our findings reveal that upregulation of RMRP may aggravate myocardial I/R injury possible by downregulation of miR-206 and subsequently upregulation of ATG3. Activation of PI3K/Akt/mTOR pathway may be a key downstream mechanism mediating the cardioprotection of RMPR/miR-206/ATG3 axis against myocardial I/R injury.