BIOTECHNOLOGY AND APPLIED BIOCHEMISTRY
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2021
·Vol. 69
·期 6
·2561-2572
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IF 2.431
Yongjun Xia,Caiyun Yang,Xiaofeng Liu,Guangqiang Wang,Zhiqiang Xiong,Xin Song,Yijin Yang,Hui Zhang,Lianzhong Ai
There have been many studies on the activities and polysaccharide production of Sanghuangporus vaninii . However, few studies have looked at triterpene production from S. vaninii using liquid-state fermentation. A method for enhancing the production of triterpenes by in situ extractive fermentation (ISEF) was studied. Eight solvents were investigated as extractants for triterpene production in the ISEF system. The results showed that using vegetable oil as an extractant significantly increased the yield of total triterpenes and biomass of S. vaninii YC-1, reaching 18.98 ± 0.71 and 44.67 ± 2.21 g/L, respectively. In 5 L fermenter experiments, the added vegetable oil improved the dissolved oxygen condition of the fermentation broth and promoted the growth of S. vaninii YC-1. Furthermore, adding vegetable oil increased the expression of fatty acid synthesis-related genes such as FAD2 and SCD , thereby increasing the synthesis of unsaturated fatty acids in the cell membrane of S. vaninii YC-1. Therefore, the cell membrane permeability of S. vaninii YC-1 increased by 19%. Our results indicated that vegetable oil increased the permeability of S. vaninii YC-1 cell membranes to promote the production of total triterpenes. The use of vegetable oil as an extractant was thus effective in increasing the yield of triterpenes in the ISEF system.
研究领域:
微生物学
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生物技术
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药用真菌研究
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DOI
PubMed
高影响因子
ORGANIC & BIOMOLECULAR CHEMISTRY
·
2015
·Vol. 13
·期 26
·7257-7264
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IF 3.562
Juan Xiao,Chunmei Jin,Zhixue Liu,Shujing Guo,Xiaochuan Zhang,Xin Zhou,Xue Wu
1-Benzyl-3-(substituted aryl)-5-methylfuro[3,2-c]pyrazole (YC-1) is a well-known synthetic compound with various satisfactory pharmacological activities, such as the activation of soluble guanylate cyclase (sGC) and the inhibition of hypoxia-induced factor-1α (HIF-1α). Recently, YC-1 has been demonstrated to have a potent activity on anti-fibrotic activity. However, the mechanism underlying its anti-fibrotic activity is still largely unknown. To this end, we presented here the design and synthesis of YC-1 and its novel derivatives, as well as the evaluation of their anti-fibrotic effects on activated human hepatic stellate cells (HSCs) LX-2. Moreover, the possible underlying mechanism of anti-fibrotic activity was also investigated for the first time by means of a CCK-8 assay, cell apoptosis analysis, and western blot analysis. Our study revealed that YC-1 and its derivatives suppressed activated LX-2 cell viability and induced cell apoptosis in a time- and dose-dependent manner. Western blot data demonstrated that these derivatives not only decreased the expression of α-smooth muscle actin (α-SMA), but also increased the expression of caspase-3, resulting in cell apoptosis. These findings strongly indicated that YC-1 and its derivatives, especially AC, could significantly inhibit LX-2 cell activation and induce LX-2 cell apoptosis by inhibiting α-SMA protein expression and promoting caspase-3 expression, respectively. In summary, our findings suggested that YC-1 derivatives might be potential agents for hepatic fibrosis therapy.
研究领域:
药理学
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细胞生物学
·
分子生物学
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DOI
PubMed
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
·
2023
·
IF 5.1
Huijuan Ma,Qi Shu,Peiyao Wang,Ruilin Qin,Sijia Li,Huan Xu
Exposure to formaldehyde (FA) has been indicated to be positively correlated with increased incidence of allergic asthma in many epidemiological and experimental studies. However, few studies have ever addressed the molecular basis of the correlation. In the present study, it was found that inhaling 2.0 mg/m 3 FA for 2 weeks could exacerbate the pulmonary inflammation and mucus over-accumulation in OVA-induced murine asthmatic model. The pro-inflammatory cytokines, such as IL-1β, TNF-α, IL-6 and IL-8, were increased in lung and serum of FA-exposed asthmatic mice. The contribution of HIF-1α signaling in FA-exacerbated allergic asthma was confirmed by bioinformatic analysis. HIF-1α and its downstream proteins, which are known as mediators of glycolysis, were found to be upregulated by 50 μM FA, and the FA-enhanced of glycolysis was reversed by inhibition of HIF-1α with PX-478 in vitro and YC-1 in vivo . Furthermore, it was confirmed that inhibition of HIF-1α signaling could restrain the macrophagic inflammatory responses and asthma exacerbation induced by FA. Collectively, these results revealed that FA could exacerbate asthma through the potentiation of HIF-1α-mediated inflammatory responses in macrophages, which also indicated the universal roles of FA-triggered macrophage metabolic and functional alterations in inflammatory or allergic diseases.
研究领域:
免疫学
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呼吸病学
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毒理学
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产品关联
DOI
PubMed
高影响因子
ACS Nano
·
2024
·
IF 15.8
Panpan Xue,Huilan Zhuang,Sijie Shao,Tingjie Bai,Xuemei Zeng,Shuangqian Yan
The activation of cellular ferroptosis is promising in tumor therapy. However, ferroptosis is parallelly inhibited by antiferroptotic substances, including glutathione peroxidase 4 (GPX4), dihydroorotate dehydrogenase (DHODH), and ferroptosis suppressor protein 1 (FSP1). Thus, it is highly desirable, yet challenging, to simultaneously suppress these three antiferroptotic substances for activating ferroptosis. Here, we rationally designed a hollow iron-doped SiO2-based nanozyme (FeSHS) loaded with brequinar (BQR) and lificiguat (YC-1), named FeSHS/BQR/YC-1-PEG, for tumor ferroptosis activation. FeSHS were developed through the continuous etching of SiO2 nanoparticles by iron ions, which exhibit pH/glutathione-responsive biodegradability, along with mimicking the activities of peroxidase, glutathione oxidase, and NAD(P)H oxidase. Specifically, glutathione depletion and NAD(P)H oxidation by FeSHS will suppress the expression of GPX4 and inhibit FSP1 by disrupting the NAD(P)H/FSP1/ubiquinone axis. In addition, the released BQR can suppress the expression of DHODH. Meanwhile, YC-1 is able to increase the cellular polyunsaturated fatty acids (PUFAs) by destroying the HIF-1α/lipid droplet axis. The elevation of levels of iron and PUFAs while simultaneously disrupting the GPX4/DHODH/FSP1 inhibitory pathways by our designed nanoplatform displayed high therapeutic efficacy both in vitro and in vivo. This work elucidates rationally designing smart nanoplatforms for ferroptosis activation and future tumor treatments.
研究领域:
纳米技术
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癌症治疗
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生物化学
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材料科学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
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