171 research outputs found

    Raw data of this article.

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    Although palmitoleic acid (POA) is a lipokine with beneficial effects on obesity and is produced as a byproduct from the manufacture of prescription omega-3 fatty acids, its role in nervous system inflammation is still unknown. This study aims to examine the mechanisms and protective effects of POA against palmitic acid (PA)-induced microglial death. PA-induced microglial death was used as a model for POA intervention. Various inhibitors were employed to suppress potential routes of PA entry into the cell. Immunofluorescence staining and Western blotting were conducted to elucidate the protective pathways involved. The results suggest POA has the potential to eliminate PA-induced lactate dehydrogenase (LDH) release, which decreases the overall number of propidium iodide (PI)-positive cells compared with control. Moreover, POA has the potential to significantly increase lipid droplets (LDs) in the cytoplasm, without causing any lysosomal damage. POA inhibited both canonical and non-canonical gasdermin D (GSDMD)-mediated pyroptosis and gasdermin E (GSDME)-mediated pyroptosis, which PA typically induces. Additionally, POA inhibited the endoplasmic reticulum (ER) stress and apoptosis-related proteins induced by PA. Based on the findings, POA can exert a protective effect on microglial death induced by PA via pathways related to pyroptosis, apoptosis, ER stress, and LDs.</div

    Original images for blots and gels.

    No full text
    Although palmitoleic acid (POA) is a lipokine with beneficial effects on obesity and is produced as a byproduct from the manufacture of prescription omega-3 fatty acids, its role in nervous system inflammation is still unknown. This study aims to examine the mechanisms and protective effects of POA against palmitic acid (PA)-induced microglial death. PA-induced microglial death was used as a model for POA intervention. Various inhibitors were employed to suppress potential routes of PA entry into the cell. Immunofluorescence staining and Western blotting were conducted to elucidate the protective pathways involved. The results suggest POA has the potential to eliminate PA-induced lactate dehydrogenase (LDH) release, which decreases the overall number of propidium iodide (PI)-positive cells compared with control. Moreover, POA has the potential to significantly increase lipid droplets (LDs) in the cytoplasm, without causing any lysosomal damage. POA inhibited both canonical and non-canonical gasdermin D (GSDMD)-mediated pyroptosis and gasdermin E (GSDME)-mediated pyroptosis, which PA typically induces. Additionally, POA inhibited the endoplasmic reticulum (ER) stress and apoptosis-related proteins induced by PA. Based on the findings, POA can exert a protective effect on microglial death induced by PA via pathways related to pyroptosis, apoptosis, ER stress, and LDs.</div

    POA protects against PA-induced cell death via the ER stress and apoptotic pathways.

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    (A, B) Cells were treated with BSA, 200 μM PA, 200 μM PA+200 μM POA for four hours, and protein levels of PERK, ATF-3, PUMA, cleaved caspase-3 (c-casp3), PARP, cleaved PARP (c-PARP) were detected via Western blot. (C-H) Immunofluorescence staining of Cyt c (green) merged with DAPI (blue). Data are shown as mean ± SD. *p p p p < 0.0001. Scale bar: 20 μm.</p

    POA protects from PA injury.

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    (A) BV-2 cells were pretreated with inhibitors or vehicles for one hour, followed by treatment with BSA for 24 h for cell viability assay. (B) BV-2 cells were pretreated with inhibitors or vehicles for one hour, followed by treatment with PA for 24 h for cell viability assay. (C) Effect of POA on BV-2 cell viability at different concentrations. (D) Effect of different POA:BSA ratios on BV-2 cell viability. (E) PA induced effect of POA on LDH release from BV-2 cells. (F-H) PI staining (red) of cells treated with BSA, 200 μM PA, 200 μM PA+200 μM POA for four hours. (I-K) PI staining merged with DAPI (blue). Data are shown as mean ± SD. *p p p p < 0.0001. Scale bar: 100 μm.</p

    POA-induced LDs may be the protective mechanism.

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    (A-C) Representative images of BODIPY staining. (D-L) Cells were treated with BSA, 200 μM PA, 200 μM PA+200 μM POA for four hours, and immunofluorescence staining was performed for LAMP1 (red), Lipid A (green) and merged with DAPI (blue). (M-O) Representative images of galectin-3 (Gal-3) immunofluorescence staining. (P-R) Representative images of cPLA2 immunofluorescence staining. (S-U) The percentage of LDs, Gal-3 and cPLA2 in the different group. Data are shown as mean ± SD. **p p < 0.001. Scale bar: 20 μm.</p

    POA protects PA-induced cell death via pyroptotic pathways.

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    (A, B) Cells were treated with BSA, 200 μM PA, 200 μM PA+200 μM POA for four hours, and protein levels of cleaved caspase-11 (c-casp11), GSDMD-N, NLRP3, ASC, cleaved caspase-1 (c-casp1), cleaved IL-1β (c-IL 1β), GSDME-N were subsequently detected by Western blot. (C, D) Concentrations of IL-1β and IL-18 in cell culture supernatants were determined via ELISA. Data are shown as mean ± SD. *p p p p < 0.0001.</p

    Mechanistic model of the protective effect of POA on PA-induced microglia death.

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    Mechanistic model of the protective effect of POA on PA-induced microglia death.</p

    POA protects against PA-induced apoptosis.

    No full text
    Although palmitoleic acid (POA) is a lipokine with beneficial effects on obesity and is produced as a byproduct from the manufacture of prescription omega-3 fatty acids, its role in nervous system inflammation is still unknown. This study aims to examine the mechanisms and protective effects of POA against palmitic acid (PA)-induced microglial death. PA-induced microglial death was used as a model for POA intervention. Various inhibitors were employed to suppress potential routes of PA entry into the cell. Immunofluorescence staining and Western blotting were conducted to elucidate the protective pathways involved. The results suggest POA has the potential to eliminate PA-induced lactate dehydrogenase (LDH) release, which decreases the overall number of propidium iodide (PI)-positive cells compared with control. Moreover, POA has the potential to significantly increase lipid droplets (LDs) in the cytoplasm, without causing any lysosomal damage. POA inhibited both canonical and non-canonical gasdermin D (GSDMD)-mediated pyroptosis and gasdermin E (GSDME)-mediated pyroptosis, which PA typically induces. Additionally, POA inhibited the endoplasmic reticulum (ER) stress and apoptosis-related proteins induced by PA. Based on the findings, POA can exert a protective effect on microglial death induced by PA via pathways related to pyroptosis, apoptosis, ER stress, and LDs.</div

    Optimization of Alkyl Side Chain Length in Polyimide for Gate Dielectrics to Achieve High Mobility and Outstanding Operational Stability in Organic Transistors

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    Alkyl chain modification strategies in both organic semiconductors and inorganic dielectrics play a crucial role in improving the performance of organic thin-film transistors (OTFTs). Polyimide (PI) and its derivatives have received extensive attention as dielectrics for application in OTFTs because of flexibility, high-temperature resistance, and low cost. However, low-temperature solution processing PI-based gate dielectric for flexible OTFTs with high mobility, low operating voltage, and high operational stability remains an enormous challenge. Furthermore, even though di-n-decyldinaphtho[2,3-b:2′,3′-f]thieno[3,2-b]thiophene (C10-DNTT) is known to have very high mobility as an air-stable and high-performance organic semiconductor, the C10-DNTT-based TFTs on the PI gate dielectrics still showed relatively low mobility. Here, inspired by alkyl side chain engineering, we design and synthesize a series of PI materials with different alkyl side chain lengths and systematically investigate the PI surface properties and the evolution of organic semiconductor morphology deposited on PI surfaces during the variation of alkyl side chain lengths. It is found that the alkyl side chain length has a critical influence on the PI surface properties, as well as the grain size and molecular orientation of semiconductors. Good field-effect characteristics are obtained with high mobilities (up to 1.05 and 5.22 cm2/Vs, which are some of the best values reported to date), relatively low operating voltage, hysteresis-free behavior, and high operational stability in OTFTs. These results suggest that the strategy of optimizing alkyl side-chain lengths opens up a new research avenue for tuning semiconductor growth to enable high mobility and outstanding operational stability of PI-based OTFTs
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