Pyridine vapor annealing induced reversible switching emission and enhanced electroluminescent performance of poly(fluorene-co-dibenzothiophene-S,S-dioxide)

Junfei Liang,Tong Wu,Jun Chen 대한금속·재료학회 2024 ELECTRONIC MATERIALS LETTERS Vol.20 No.2

In this article, we report on blue-green exciplex emission through pyridine solvent vapor annealing blue-light polymerPFSO10, which is comprised the strong electron-withdrawing dibenzo-thiophene- S , S -dioxide with the molar ratio of 10%. The photoluminescent spectrum of PFSO10 fi lm emerged a fresh low-energy emission peaked at 482 nm after pyridinesolvent vapor annealing, which was stemmed from the exciplex charge-transfer state between the PFSO10 and pyridine. It isworth noting that the exciplex emission peaked at 482 nm from the pyridine solvent vapor annealing fi lm was disappearedafter thermal annealed at 120 °C and its photoluminescent spectrum was similar to that of the pristine PFSO10 fi lm. Thissimilar phenomenon of photoluminescent spectrum was also occurred to the electroluminescent spectra of the PFSO10fi lms. Furthermore, the device performance of PFSO10 was achieved signifi cant improvement after pyridine solvent vaporannealing. With optimizing the pyridine vapor annealing process, the device based on PFSO10 as emissive layer receiveda maximum luminous effi ciency of 6.74 cd A −1 with the peak brightness of 22,364 cd m −2 , which was enlarged over 140%compared to that of 2.77 cd A −1 for the pristine PFSO10. These results demonstrate that appropriate solvent vapor annealingcan be a simple and eff ective strategy to realize the reversible switching emission and improve the device performance.

Ginseng improves cognitive deficit via the RAGE/NF-kB pathway in advanced glycation end product-induced rats

Xiaobin Tan,Junfei Gu,Bingjie Zhao,Shuyuan Wang,Jiarui Yuan,Chunfei Wang,Juan Chen,Jiping Liu,Liang Feng,Xiaobin Jia 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.2

Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent andtreat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such asAlzheimer’s disease (AD). The present study evaluated the neuroprotective effects of PG and its possibleneuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats’brains. The Morris water maze test and step-down type passive avoidance test were performed toevaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products(RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-kB). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened theescape latency, remarkably increased the number of crossing times, significantly decreased the numberof errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantlyreduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutaseactivity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE andNF-kB. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments andregulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairmentand attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may beassociated with the RAGE/NF-kB pathway. Our results provided the experimental basis for applying PG inpreventing and treating AD.

Ginseng improves cognitive deficit via the RAGE/NF-κB pathway in advanced glycation end product-induced rats

Tan, Xiaobin,Gu, Junfei,Zhao, Bingjie,Wang, Shuyuan,Yuan, Jiarui,Wang, Chunfei,Chen, Juan,Liu, Jiping,Feng, Liang,Jia, Xiaobin The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.2

Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent and treat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such as Alzheimer's disease (AD). The present study evaluated the neuroprotective effects of PG and its possible neuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats' brains. The Morris water maze test and step-down type passive avoidance test were performed to evaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products (RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-${\kappa}B$). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened the escape latency, remarkably increased the number of crossing times, significantly decreased the number of errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantly reduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutase activity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE and NF-${\kappa}B$. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments and regulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairment and attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may be associated with the RAGE/NF-${\kappa}B$ pathway. Our results provided the experimental basis for applying PG in preventing and treating AD.

Suppression of SPARC Ameliorates Ovalbumin-induced Airway Remodeling via TGFβ1/Smad2 in Chronic Asthma

Pan Yun,Zhang Dong,Zhang Jintao,Liu Xiaofei,Xu Jiawei,Zeng Rong,Cui Wenjing,Liu Tian,Wang Junfei,Dong Liang 대한천식알레르기학회 2024 Allergy, Asthma & Immunology Research Vol.16 No.1

Purpose: Airway remodeling is a critical feature of asthma. Secreted protein acidic and rich in cysteine (SPARC), which plays a cardinal role in regulating cell-matrix interactions, has been implicated in various fibrotic diseases. However, the effect of SPARC in asthma remains unknown. Methods: We studied the expression of SPARC in human bronchial epithelial cells and serum of asthmatics as well as in the lung tissues of chronic asthma mice. The role of SPARC was examined by using a Lentivirus-mediated SPARC knockdown method in the ovalbumin (OVA)-induced asthma mice. The biological processes regulated by SPARC were identified using RNA sequencing. The function of SPARC in the remodeling process induced by transforming growth factor β1 (TGFβ1) was conducted by using SPARC small interfering RNA (siRNA) or recombinant human SPARC protein in 16HBE cells. Results: We observed that SPARC was up-regulated in human bronchial epithelia of asthmatics and the asthmatic mice. The levels of serum SPARC in asthmatics were also elevated and negatively correlated with the forced expiratory volume in one second (FEV1) to forced vital capacity ratio (FVC) (r = −0.485, P < 0.01) and FEV1 (%predicted) (r = −0.425, P = 0.001). In the chronic asthmatic mice, Lentivirus-mediated SPARC knockdown significantly decreased airway remodeling and airway hyper-responsiveness. According to gene set enrichment analysis, negatively enriched pathways found in the OVA + short hairpin-SPARC group included ECM organization and collagen formation. In the lung function studies, knockdown of SPARC by siRNA reduced the expression of remodeling-associated biomarkers, cell migration, and contraction by blocking the TGFβ1/Smad2 pathway. Addition of human recombinant SPARC protein promoted the TGFβ1-induced remodeling process, cell migration, and contraction in 16HBE cells via the TGFβ1/Smad2 pathway. Conclusions: Our studies provided evidence for the involvement of SPARC in the airway remodeling of asthma via the TGFβ1/Smad2 pathway.