FASEB JOURNAL
·
2025
·Vol. 39
·期 5
·e70420
·
IF 4.2
Min Zhu,Xiaofang Fan,Nan Zhang,Hui Wang,Jianshe Ma,Xianghong Yin,Junyan Cai,Linjing Cong,Ran Chen,Junming Fan,Xiaoxia Kong,Bin Geng,Yongsheng Gong,Congkuo Du
Endothelial pyroptosis, a pro-inflammatory programmed cell death, promotes endothelial inflammation and is a pivotal process in the initial stage of acute lung injury (ALI). Hydrogen sulfide (H 2 S), a gasotransmitter primarily dependent on cystathionine γ-lyase (CSE) in the cardiovascular and respiratory systems, plays a protective role during ALI. Nonetheless, the modulatory role and precise molecular mechanism of endothelial endogenous CSE/H 2 S in the pathogenesis of ALI remain elusive. Herein, we prepared an ALI mouse model using intratracheal administration of LPS (5 mg/kg), and lung injury was assessed by evaluating pulmonary edema, inflammatory response, and endothelial pyroptosis. In this model, H 2 S production from pulmonary tissues declined in a time-dependent manner, accompanied by a compensatory elevation of CSE protein levels. Treatment with the H 2 S donor (NaHS) attenuated pulmonary edema, inflammatory cell infiltration, endothelial pyroptosis, and reduced serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Meanwhile, the inducible deletion of CSE in endothelial cells exacerbated these changes. The blocking effect of CSE/H 2 S on endothelial pyroptosis (evidenced by caspase-11 activation and GSDMD-NT formation) was also confirmed in cultured pulmonary microvascular endothelial cells (PMECs). Mechanistically, H 2 S-mediated regulation of sirtuin-1 (SIRT1) expression and activation (via sulfhydration) contributed to the modulatory process. Collectively, we uncovered that endothelial endogenous CSE/H 2 S alleviates endothelial pyroptosis by activating SIRT1, thereby preventing LPS-induced acute lung injury. Graphical In the LPS-induced ALI model, caspase-1-independent pyroptosis was activated. The expression of activated caspase-11 and GSDMD-NT was increased, accompanied by pulmonary edema and inflammatory infiltration. Endothelial CSE/H 2 S deficiency aggravated endothelial pyroptosis and acute lung injury. Mechanistically, endothelial endogenous CSE/H 2 S mediated the expression and activation of sirtuin-1 (SIRT1) via sulfhydration, one of the post-translational modifications. Activated SIRT1 inhibited the activation of caspase-11 and GSDMD-NT to inhibit endothelial pyroptosis, thereby alleviating acute lung injury.
研究领域:
医学
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分子生物学
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DOI
PubMed
高影响因子
EUROPEAN POLYMER JOURNAL
·
2021
·
IF 4.598
Qilong Li,Na Li,Xiangqiang Pan,Jian Zhu
To investigate the complexity of breaking aryl C Se bond, alkyl C Se bond and alkyl C S bond by ultraviolet light, three maleimide polymers are employed as objects, including SePhP which reported in our previous work having aryl C Se bond, SePP which synthesized via radical copolymerization of N -(4-selenophenyl)-propyl maleimide and styrene having alkyl C Se bond and SPP which synthesized via radical copolymerization of N -(4-thiophenyl)-propyl maleimide and styrene having alkyl C S bond. After careful structure characteristics, SePhP, SePP and SPP are treated by ultraviolet light, as a result, only C Se bond of SePP can be broken. When SePP is irradiated by ultraviolet light in an oxygen-free condition, it can make a structure change from linear to cross-linked and refractive index decrease of polymer. Furthermore, utilizing photo-crosslinking and changing of refractive index of SePP after ultraviolet light irradiation, we realize visual photomask patterning in a simple system, which will bring great potential in display devices, anti-counterfeit labels, and etc.
研究领域:
材料科学
·
化学
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DOI
高影响因子
VETERINARY RESEARCH
·
2023
·Vol. 54
·期 1
·1-12
·
IF 4.4
Fu Shaodong,Wang Zhenglei,Han Xiangan,Xu Yuanyuan,Miao Jinfeng
Macrophages play a pivotal role in the inflammatory response to the zoonotic pathogen E. coli, responsible for causing enteric infections. While considerable research has been conducted to comprehend the pathogenesis of this disease, scant attention devoted to host-derived H2S. Herein, we reported that E. coli infection enhanced the expression of CSE in macrophages, accompanied by a significantly increased inflammatory response. This process may be mediated by the involvement of excessive autophagy. Inhibition of AMPK or autophagy with pharmacological inhibitors could alleviate the inflammation. Additionally, cell model showed that the mRNA expression of classic inflammatory factors (Il-1β, Il-6), macrophage polarization markers (iNOS, Arg1) and ROS production was significantly down-regulated after employing CSE specific inhibitor PAG. And PAG is capable of inhibiting excessive autophagy through the LKB1-AMPK-ULK1 axis. Interestingly, exogenous H2S could suppress inflammation response. Our study emphasizes the importance of CSE in regulating the macrophage-mediated response to E. coli. Increased CSE in macrophages leads to excessive inflammation, which should be considered a new target for drug development to treat intestinal infection.
研究领域:
免疫学
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微生物学
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药理学
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DOI
PubMed
高影响因子
MOLECULAR NUTRITION & FOOD RESEARCH
·
2024
·
IF 4.5
Kelin Li,Victoria A. Uyanga,Xiaojuan Wang,Hongchao Jiao,Jingpeng Zhao,Yunlei Zhou,Haifang Li,Hai Lin
Scope Allicin, a product of enzymatic reaction when garlic is injured, plays an important role in maintaining glucose homeostasis in mammals. However, the effect of allicin on glucose homeostasis in the state of insulin resistance remains to be elucidated. This study investigates the effect of allicin on glucose metabolism using different muscle fibers in a chicken model. Methods and results Day-old male Arbor Acres broilers are randomly divided into three groups and fed a basal diet supplemented with 0, 150, or 300 mg kg −1 allicin for 42 days. Results show that allicin improves the zootechnical performance of broilers at the finishing stage. The glucose loading test (2 g kg −1 body mass) indicates the regulatory role of allicin on glucose homeostasis. In vitro results demonstrate allicin increases glutathione (GSH) level and the expression of cystathionine γ lyase (CSE), leading to endogenous hydrogen sulfide (H 2 S) production in M. pectoralis major (PM) muscle-derived myotubes. Allicin stimulates adenosine monophosphate-activated protein kinase (AMPK) S-sulfhydration and AMPK phosphorylation to promote glucose uptake, which is suppressed in the presence of d , l -propargylglycine (PAG, a CSE inhibitor). Conclusion This study demonstrates that allicin induces AMPK S-sulfhydration and AMPK phosphorylation to promote glucose uptake via the CSE/H 2 S system in a muscle fiber-dependent manner.
研究领域:
动物科学
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营养学
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分子生物学
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DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2019
·
IF 3.743
Zhongchao Wang,Ying Yan,Yini Wang,Fei Tong
Introduction The purpose of the experiment was to survey the therapeutic function of resveratrol (RES)-loaded poly(ethylene glycol)-poly(phenylalanine) (PEG-PPhe) on intestinal ischemia/reperfusion injury (II/RI) via the interaction between CSE/H 2 S and iNOS/NO compared to free RES in diabetic rats. Methods Diabetic rats were pretreated with 20 mg/kg of RES or the RES/PEG-PPhe complex and then subjected to 1 h of ischemia and 3 h of reperfusion. Blood and intestines were collected, intestinal pathological injury was estimated, and the contents of body weight, weights of different tissues, blood glucose, serum insulin, HOMA index, serum nitric oxide (NO) and serum sulfureted hydrogen (H 2 S) were observed. The dry/wet intestine ratios, the activity of superoxide dismutase (SOD); the contents of methane dicarboxylic aldehyde (MDA), glutathione (GSH), H 2 S, and NO; and the concentrations of inducible nitric oxide synthase (iNOS) and cystathionine-γ-lyase (CSE) were observed in the intestinal tissues. Results A significant reduction of weights of different tissues, blood glucose, pathological damage, dry/wet ratios, MDA, NO, iNOS expression and a significant increasement of body weight, serum insulin, HOMA index, SOD, GSH, H 2 S, CSE expression were observed in both treatment groups. However, a greater reduction of weights of different tissues, blood glucose (7.49–13.49 mmol/L for 72 h vs. the control) and pathological damage, iNOS expression, dry/wet ratios (6.14 ± 0.29 vs. 8.51 ± 0.42), MDA (5.01 ± 0.71 nmol vs. 9.98 ± 0.67 nmol), NO (0.52 ± 0.09 μmol vs. 0.99 ± 0.08 μmol in intestinal tissue; 19.29 ± 0.89 μmol vs. 45.23 ± 1.17 μmol in serum) was observed in the RES/PEG-PPhe group relative to the I/R ( P < 0.01 for all); a greater increasement of body weight, serum insulin, HOMA index, SOD (39.79±1.78 U vs. 11.84 ± 1.02 U), GSH (31.25 ± 1.19 mg vs. 10.13 ± 0.64 mg), H 2 S (39.52 ± 1.32 nmol vs. 13.02 ± 1.03 nmol in intestinal tissue; 9.78 ± 0.79 μmol vs. 3.11 ± 0.85 μmol in serum), CSE expression was observed in the RES/PEG-PPhe group relative to the I/R ( P < 0.01 for all). In addition, aminoguanidine (AMI, iNOS inhibitor) reduced I/R injury, and dl -propargylglycine (PAG, CSE inhibitor) increased I/R injury. Conclusions The interaction between CSE/H2S and the iNOS/NO-mediated resveratrol/poly(ethylene glycol)-poly(phenylalanine) complex alleviates intestinal ischemia/reperfusion injuries in diabetic rats.
研究领域:
药理学
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医学
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分子生物学
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糖尿病研究
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产品关联
DOI
PubMed
高影响因子
International Journal of Nanomedicine
·
2018
·
IF 4.37
Fei Tong,Rongkui Chai,Haiying Jiang,Bo Dong
Background The objective of this study was to survey the therapeutic function of curcumin-encapsulated poly(gamma-benzyl l-glutamate)-poly(ethylene glycol)-poly(gammabenzyl l-glutamate) (PBLG-PEG-PBLG) (P) on diabetic cardiomyopathy (DCM) via cross regulation effect of calcium-sensing receptor (CaSR) and endogenous cystathionine-γ-lyase (CSE)/hydrogen sulfide (H 2 S). Methods Diabetic rats were preconditioned with 20 mg/kg curcumin or curcumin/P complex continuously for 8 weeks. The blood and myocardiums were collected, the level of serum H 2 S was observed, and the [Ca 2+ ] i content was measured in myocardial cells, and hematoxylin-eosin, CaSR, CSE, and calmodulin (CaM) expression were detected. Results Both curcumin and curcumin/P pretreatment alleviated pathological morphological damage of myocardium, increased H 2 S and [Ca 2+ ] i levels, and upregulated the expression of CaSR, CSE, and CaM as compared to DCM group, while curcumin/P remarkably augmented this effect. Conclusion PBLG-PEG-PBLG could improve water-solubility and bioactivity of curcumin and curcumin/PBLG-PEG-PBLG significantly alleviated diabetic cardiomyopathy.
研究领域:
药理学
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心血管疾病
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纳米医学
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产品关联
DOI
PubMed
高影响因子
Toxicology Research
·
2022
·Vol. 11
·期 2
·374-384
·
IF 2.68
Yang Bobo,Yin Changsheng,Zhang Yu,Xing Guangwei,Wang Suhua,Li Fang,Aschner Michael,Lu Rongzhu
BackgroundHydrogen sulfide (H2S), as the third gasotransmitter participates in both cellular physiological and pathological processes, including chemical-induced injuries. We recently reported acute acrylonitrile (AN) treatment inhibited endogenous H2S biosynthesis pathway in rat and astrocyte models. However, there is still no evidence to address the correlation between endogenous H2S and sub-chronic AN exposure.ObjectivesThis study aims to explore the modulatory effects of prolonged AN exposure on endogenous H2S levels and its biosynthetic enzymes in rat blood, brain and liver.MethodsA total of 50 male Sprague-Dawley rats were randomly divided into 5 groups, including the control group and AN-treated groups at dosages of 6.25, 12.5, 25 or 50 mg/kg. Rats received one exposure/day, 5 days/week, for 4 consecutive weeks. The rat bodyweight and brain/liver organ coefficient were detected, along with liver cytochrome P450 2E1(CYP2E1) expression. In addition, the H2S contents in rat serum and plasma, and in cerebral cortex and liver tissues were measured by methylene blue method. The expression of H2S-generating enzymes, including cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MPST) was also measured with Western blot both in rat cerebral cortex and liver.ResultsSubchronic exposure to AN significantly inhibited bodyweight-gain and increased the liver CYP2E1 expression compared with the control. In addition, AN significantly increased H2S levels in rat plasma and serum, but not in liver. The endogenous H2S level in rat cerebral cortex was also significantly increased upon AN treatment, when expression of the major H2S-generating enzymes, CBS and 3-MPST were significantly enhanced. However, hepatic protein levels of CBS and CSE were significantly increased, whereas hepatic levels of 3-MPST were significantly decreased.ConclusionThis study showed that sub-chronic AN exposure increased endogenous H2S contents in rat blood and brain tissues, but not liver, which may be resulted from the distinct expression profile of H2S-producing enzymes in response to AN. The blood H2S contents may be applied as a potential novel biomarker for surveillance of chronically AN-exposed populations.HighlightsSubchronic intraperitoneal exposure to acrylonitrile increased H2S content in rat blood and cerebral cortex, but not in liver.Distinct tissue expression profiles of H2S-producing enzymes contribute to the acrylonitrile-induced differential effects on the H2S level.Blood H2S level may be a biomarker for subchronic exposure to acrylonitrile.
研究领域:
毒理学
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药理学
·
生物化学
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DOI
PubMed
高影响因子
Oxidative Medicine and Cellular Longevity
·
2019
·
IF 4.868
Ruxia Wang,Kelin Li,Hui Wang,Hongchao Jiao,Xiaojuan Wang,Jingpeng Zhao,Hai Lin
Aims. Insulin and glucocorticoids play crucial roles in skeletal muscle protein turnover. Fast-twitch glycolytic fibres are more susceptible to atrophy than slow-twitch oxidative fibres. Based on accumulating evidence, hydrogen sulfide (H2S) is a physiological mediator of this process. The regulatory effect of H2S on protein synthesis in fast-twitch fibres was evaluated. Results. A NaHS (sodium hydrosulfide) injection simultaneously increased the diameter of M. pectoralis major (i.e., fast-twitch glycolytic fibres) and activated the mammalian target of the rapamycin (mTOR)/p70S6 kinase (p70S6K) pathway. Dexamethasone (DEX) inhibited protein synthesis, downregulated mTOR and p70S6K phosphorylation, and suppressed the expression of the cystathionine γ-lyase (CSE) protein in myoblasts. The precursor of H2S, L-cysteine, completely abolished the inhibitory effects of DEX. The CSE inhibitor DL-propargylglycine (PAG) completely abrogated the effects of RU486 on blocking the suppressive effects of DEX. The H2S donor NaHS increased the H2S concentrations and abrogated the inhibitory effects of DEX on protein synthesis. Insulin increased protein synthesis and upregulated CSE expression. However, PAG abrogated the stimulatory effects of insulin on protein synthesis and the activity of the mTOR/p70S6K pathway. Innovation. These results demonstrated that CSE/H2S regulated protein synthesis in fast-twitch muscle fibres, and glucocorticoids and insulin regulated protein synthesis in an endogenous CSE/H2S system-dependent manner. Conclusions. The results from the present study suggest that the endogenous CSE/H2S system regulates fast-twitch glycolytic muscle degeneration and regeneration.
研究领域:
药理学
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生理学
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分子生物学
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内分泌学
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 4.7
Zhenshuai Zhang,Li Jiang,Lu Chen,Xinyan Cai,Yuteng Wang,Wenqian Xue,Kaijian Lei,Tianxiao Wang
Colorectal cancer (CRC) remains one of the most prevalent malignancies globally, with limited therapeutic options for advanced-stage patients due to acquired drug resistance and systemic toxicity. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising therapeutic target for CRC, while cystathionine γ-lyase (CSE)—a key enzyme in hydrogen sulfide (H 2 S) biosynthesis—plays a critical role in maintaining redox homeostasis and suppressing ferroptosis in cancer cells. Here, we synthesized a novel small-molecule compound, DPhA-EtOBz-TSC, and systematically evaluated its anti-CRC efficacy and underlying molecular mechanism. The chemical structure of DPhA-EtOBz-TSC was confirmed by 1 H nuclear magnetic resonance ( 1 H NMR), 13 C NMR, and high-resolution mass spectrometry (HRMS). In vitro studies using human CRC cell lines (HCT8 and SW480) demonstrated that DPhA-EtOBz-TSC specifically targeted and inhibited CSE: molecular docking and cellular thermal shift assay (CETSA) confirmed direct binding between DPhA-EtOBz-TSC and CSE (binding affinity ΔG = −29.07 ± 3. 85 kcal/mol), while Western blot analysis revealed a concentration-dependent reduction in CSE protein levels in SW480 and HCT8 cells treated with DPhA-EtOBz-TSC. Mechanistically, DPhA-EtOBz-TSC-induced CSE downregulation disrupted the CSE-H 2 S-GPX4 axis, leading to reduced glutathione (GSH) levels, decreased glutathione peroxidase 4 (GPX4) activity, and accumulation of lipid reactive oxygen species (ROS) and malondialdehyde (MDA)—hallmarks of ferroptosis. Additionally, Electron microscopy and JC-1 staining revealed that DPhA-EtOBz-TSC induced significant alterations in mitochondrial morphology and a marked reduction in mitochondrial membrane potential (ΔΨm). Functionally, DPhA-EtOBz-TSC exhibited potent in vitro anti-CRC activity with IC 50 values of 25.15 μM (HCT8) and 26.11 μM (SW480) respectively, and suppressed migration and invasion. In vivo, DPhA-EtOBz-TSC (10 mg/kg/day, i.p.) significantly suppressed the growth of CT26 cell-derived xenograft tumors in BALB/c mice without causing obvious histopathological abnormalities in major organs (heart, liver, spleen, lung, kidney). Immunohistochemical staining of tumor tissues confirmed increased lipid peroxidation and decreased CSE/GPX4 expression in DPhA-EtOBz-TSC-treated mice, consistent with in vitro findings. In conclusion, DPhA-EtOBz-TSC is a novel CSE-targeting compound that induces ferroptosis in CRC cells and inhibits tumor growth in vivo. Our findings identify DPhA-EtOBz-TSC as a potential lead compound for CRC therapy and highlight the CSE-H 2 S-GPX4 axis as a viable therapeutic target for ferroptosis-based anticancer strategies.
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PubMed
高影响因子
ACS Chemical Neuroscience
·
2021
·
IF 4.418
Yang Zhang,Kexin Li,Xiangyi Wang,Yanyu Ding,Zhiruo Ren,Jinglong Fang,Tao Sun,Yan Guo,Zhiwu Chen,Jiyue Wen
The effect of cystathionine-γ-lyase (CSE)-derived hydrogen sulfide (H2S) on the reactive proliferation of astrocytes and neural functional recovery over 30 d after acute cerebral ischemia and reperfusion (I/R) was determined by applying wild-type (WT) and CSE knockout (KO) mice. The changes of glial fibrillary acidic protein (GFAP) expression in hippocampal tissues was tested. Besides, we assessed the changes of mice spatial learning memory ability, neuronal damage, RhoA, Rho kinase 2 (ROCK2), and myelin basic protein (MBP) expressions in hippocampal tissues. The results revealed that cerebral I/R resulted in obvious increase of GFAP expression in hippocampal tissues. Besides, we found the neuronal damage, learning, and memory deficits of mice induced by cerebral I/R as well as revealed the upregulation of RhoA and ROCK2 expressions and reduced MBP expression in hipppcampal tissues of mice following cerebral I/R. Not surprisingly, the GFAP expression and cerebral injury as well as the upregulation of the RhoA/ROCK2 pathway were more remarkable in CSE KO mice, compared with those in WT mice over 30 d following acute cerebral I/R, which could be blocked by NaHS treatment, a donor of exogenous H2S. In addition, the ROCK inhibitor Fasudil also inhibited the reactive proliferation of astrocytes and ameliorated the recovery of neuronal function over 30 d after cerebral I/R. For the purpose of further confirmation of the role of H2S on the astrocytes proliferation following cerebral I/R, the immunofluorescence double staining: bromodeoxyuridine (BrdU) and GFAP was evaluated. There was a marked upregulation of BrdU-labeled cells coexpressed with GFAP in hippocampal tissues at 30 d after acute cerebral I/R; however, the increment of astrocytes proliferation could be ameliorated by both NaHS and Fasudil. These findings indicated that CSE-derived H2S could inhibit the reactive proliferation of astrocytes and promote the recovery of mice neural functional deficits induced by a cerebral I/R injury via inhibition of the RhoA/ROCK2 signal pathway.
研究领域:
神经科学
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药理学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
Scientific Reports
·
2015
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IF 5.578
Ailin Xiao,Hongjuan Wang,Xin Lu,Jianchun Zhu,Di Huang,Tonghui Xu,Jianqiang Guo,Chuanyong Liu,Jingxin Li
H2S is produced mainly by two enzymes:cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE), using L-cysteine (L-Cys) as the substrate. In this study, we investigated the role of H2S in gastric accommodation using CBS(+/-) mice, immunohistochemistry, immunoblot, methylene blue assay, intragastric pressure (IGP) recording and electrical field stimulation (EFS). Mouse gastric fundus expressed H2S-generating enzymes (CBS and CSE) and generated detectable amounts of H2S. The H2S donor, NaHS or L-Cys, caused a relaxation in either gastric fundus or body. The gastric compliance was significantly increased in the presence of L-Cys (1 mM). On the contrary, AOAA, an inhibitor for CBS, largely inhibited gastric compliance. Consistently, CBS(+/-) mice shows a lower gastric compliance. However, PAG, a CSE inhibitor, had no effect on gastric compliances. L-Cys enhances the non-adrenergic, non-cholinergic (NANC) relaxation of fundus strips, but AOAA reduces the magnitude of relaxations to EFS. Notably, the expression level of CBS but not CSE protein was elevated after feeding. Consistently, the production of H2S was also increased after feeding in mice gastric fundus. In addition, AOAA largely reduced food intake and body weight in mice. Furthermore, a metabolic aberration of H2S was found in patients with functional dyspepsia (FD). In conclusion, endogenous H2S, a novel gasotransmitter, involves in gastric accommodation.
研究领域:
胃肠病学
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药理学
·
生理学
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产品关联
DOI
PubMed
高影响因子
ADVANCED FUNCTIONAL MATERIALS
·
2024
·
IF 18.5
Yaping Wang,Pengcheng Yuan,Xiong Xiong Liu,Shengfa Feng,Mufan Cao,Jianxiang Ding,Jiacheng Liu,Song-Zhu Kure-Chu,Takehiko Hihara,Long Pan,ZhengMing Sun
Composite solid electrolytes (CSEs) integrate the fast ion conductivity of inorganic electrolytes and the excellent interfacial compatibility of polymer electrolytes. Typically, fluoropolymers and garnets are promising individuals to formulate cutting-edge CSEs owing to their unique properties. However, the alkaline garnets can induce the dehydrofluorination of fluoropolymers, deteriorating their CSEs performance. Here, for the first time, NH 4 HCO 3 is proposed as a sacrificial inhibitor to effectively prevent the garnet-induced dehydrofluorination, using Li 6.4 La 3 Zr 1.4 Ta 0.6 O 12 (LLZTO) and poly(vinylidene fluoride- co -hexafluoropropylene) (PVH) as symbolic garnets and fluoropolymers, respectively. Various findings demonstrate that NH 4 HCO 3 can buffer the alkalinity of LLZTO, thereby inhibiting the dehydrofluorination of PVH. In addition, NH 4 HCO 3 can completely decompose to volatiles upon drying without compromising the properties of LLZTO and PVH. Additionally, a polymer-in-salt strategy is further introduced by adding high-concentration LiTFSI salt to the above system, resulting in the PVH/LiTFSI/LLZTO (PLL) CSEs. Benefiting from the synergetic coupling of the sacrificial inhibitor and polymer-in-salt strategies, the PLL exhibits an exceptionally high ionic conductivity of 1.2 mS cm −1 at 25 °C and stable voltage of 5.09 V, outperforming other reported CSEs. Consequently, the PLL delivers impressive high-rate cyclability in solid-state lithium-metal batteries with an outstanding capacity retention of 95.4% after 240 cycles at 1 C (25 °C).
研究领域:
材料科学
·
电化学
·
能源存储
✓ 已验证
DOI
高影响因子
危险品化学品经营许可证（带存储）