scholarly journals Down-regulated RPS-30 in Angiostrongylus Cantonensis L5 Plays a Defensive Role Against Damage Due to Oxidative Stress

2020 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Qing Shi ◽  
Yuanjiao Zhang ◽  
Junting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
Helminthic Infections ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In A. cantonensis L5 worms, down-regulated Acan-RPS-30 plays a defensive role against damage due to oxidative stress for worm survival through inhibiting apoptosis by regulating ced-3 down-regulated.

scholarly journals Down-regulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Qing Shi ◽  
Yuanjiao Zhang ◽  
Junting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
The Central Nervous System ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In C. elegans worms, down-regulated RPS-30 plays a defensive role against damage due to oxidative stress for worm survival by regulating ced-3 down-regulated. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-RPS-30 down-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

scholarly journals Down-regulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Author(s):  
Wei-Wei Sun ◽  
Xiu-Mei Yan ◽  
Qing Shi ◽  
Yuan-Jiao Zhang ◽  
Jun-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
The Central Nervous System ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30–/– mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30–/– mutant worms.Conclusion: In C. elegans worms, down-regulated RPS-30 plays a defensive role against damage due to oxidative stress for worm survival by regulating ced-3 down-regulated. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-RPS-30 down-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

scholarly journals Downregulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Wei-Wei Sun ◽  
Xiu-Mei Yan ◽  
Qing Shi ◽  
Yuan-Jiao Zhang ◽  
Jun-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
C Elegans ◽  
Defensive Role ◽  
The Central Nervous System ◽  
Rapid Amplification ◽  
Apoptosis Gene ◽  
High Level

Abstract Background Eosinophilic meningitis, caused by fifth-stage larvae of the nematode (roundworm) Angiostrongylus cantonensis, is mainly attributed to the contribution of eosinophils to tissue inflammatory responses in helminthic infections. Eosinophils are associated with the killing of helminths via peroxidative oxidation and hydrogen peroxide generated by the dismutation of superoxide produced during respiratory bursts. In contrast, when residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in the hosts. In a previous study we demonstrated that the expression of the A. cantonensis RPS 30 gene (Acan-rps-30) was significantly downregulated in A. cantonensis L5 roundworms residing in cerebrospinal fluid with a high level of eosinophils. Acan-RPS-30 is a protein homologous to the human Fau protein that plays a pro-apoptotic regulatory role and may function in protecting worms from oxidative stress. Methods The isolation and structural characterization of Acan-RPS-30 were performed using rapid amplification of cDNA ends (RACE), genome walking and bioinformatics. Quantitative real-time-PCR and microinjection were used to detect the expression patterns of Acan-rps-30. Feeding RNA interference (RNAi) was used to knockdown the apoptosis gene ced-3. Microinjection was performed to construct transgenic worms. An oxidative stress assay was used to determine the functions of Acan-RPS-30. Results Our results showed that Acan-RPS-30 consisted of 130 amino acids. It was grouped into clade V with C. elegans in the phylogenetic analysis. It was expressed ubiquitously in worms and was downregulated in both L5 larvae and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both upregulated in the transgenic worms. The phenotype susceptible to oxidative stress could be converted with a ced-3 defective mutation and RNAi. rps-30−/− mutant worms were resistant to oxidative stress, with ced-3 and ced-4 both downregulated. The oxidative stress-resistant phenotype could be rescued and inhibited by through the expression of pCe-rps30::Acan-rps-30::rfp in rps-3−/− mutant worms. Conclusion In C. elegans worms, downregulated RPS-30 plays a defensive role against damage due to oxidative stress, facilitating worm survival by regulating downregulated ced-3. This observation may indicate the mechanism by which A. cantonensis L5 worms, with downregulated Acan-RPS-30, survive in the central nervous system of humans from the immune response of eosinophils. Graphic abstract

scholarly journals Up-Regulated Galectin-1 in Angiostrongylus Cantonensis L5 Reduces Body Fat and Increases Oxidative Stress Tolerance

2021 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Aijun Qiao ◽  
Yuanjiao Zhang ◽  
Ling Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Stress Tolerance ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Lipid Deposition ◽  
Oxidative Stress Tolerance ◽  
The Central Nervous System

Abstract Background: Angiostrongylus cantonensis L5, parasitizing in human cerebrospinal fluid, leads to eosinophilic meningitis, which is attributed to tissue inflammatory responses caused primarily by high percentage of eosinophils. Eosinophils are also involved in helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival. In previous study, we have demonstrated the extracellular function of Acan-Gal-1 in inducing the apoptosis of macrophages. And here, the intracellular functions of Acan-Gal-1 were investigated with the aim to further reveal the mechanism of A. cantonensis L5 worms surviving in the central nervous system of human from inflammatory responses. Methods: Bioinformatics were used to analyse the structural characterisation of Acan-Gal-1; qRT-PCR and microinjection were performed to detect the expression patterns of Acan-gal-1; microinjection was performed to construct transgenic worms; oxidative stress assay and Oil Red O fat staining were used to determine the functions of Acan-Gal-1.Results: The results showed that Acan-Gal-1 was expressed ubiquitously and mainly localized in cuticle, and it was up-regulated in both L5 and adult worm. N2 worms expressing pCe-Acan-gal-1::Acan-gal-1::rfp, with lipid deposition reduced, were significantly resistant to oxidative stress. lec-1 mutant worms, with lipid deposition increased, showed susceptible to oxidative stress, and this phenotype could be rescued by expressing pCe-Acan-gal-1::Acan-gal-1::rfp. And fat-6;fat-7 double-mutant worms expressing pCe-Acan-gal-1::Acan-gal-1::rfp showed no significant changes in oxidative stress tolerance.Conclusion: In C. elegans worms, up-regulated Acan-Gal-1 plays a defensive role against damage due to oxidative stress for worm survival through reducing fat deposition. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-Gal-1 up-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

Oxidative Stress and Atherosclerosis: Its Relationship to Growth Factors, Thrombus Formation and Therapeutic Approaches

1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factors ◽  
Vessel Wall ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Vascular Lesion ◽  
Coagulation System ◽  
Therapeutic Approaches ◽  
Causative Relationship

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.

Serum of 8-OHdG as a potential biomarker of oxidative DNA damage in workers exposed to harmful working environments

2020 ◽  
pp. 783-783
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Blood Serum ◽  
Oxidative Dna Damage ◽  
Working Environment ◽  
Working Environments ◽  
Potential Biomarker ◽  
High Level ◽  
Damage Marker

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

scholarly journals Manipulation of Quercetin and Melatonin in the Down-Regulation of HIF-1α, HSP-70 and VEGF Pathways in Rat’s Kidneys Induced by Hypoxic Stress

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582094979
Author(s):  
Aliah R. Alshanwani ◽  
Sameerah Shaheen ◽  
Laila M. Faddah ◽  
Ahlam M. Alhusaini ◽  
Hanaa M. Ali ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Histopathological Examination ◽  
Hemoglobin Concentration ◽  
Vascular Endothelial ◽  
Hsp 70 ◽  
Reactive Protein ◽  
Defensive Role ◽  
Factor Α ◽  
Endothelial Growth Factor

Hypoxia may lead to inflammatory responses by numerous signaling pathways. This investigation intended to inspect the defensive role of Quercetin (Quer) and/ or Melatonin (Mel) against reno toxicity induced by Sodium nitrite (Sod ntr). Sod ntr injection significantly decreased blood hemoglobin concentration (Hb) with a concurrent increase in serum tumor necrosis factor- α, interleukin-6, C-reactive protein, creatinine, and urea levels. Over protein-expression of vascular endothelial growth factor and heat shock, protein-70 and mRNA of HIF-1α were also observed. Pretreatment of the Sod ntr- injected rats with the aforementioned antioxidants; either alone or together significantly improved such parameters. Histopathological examination reinforced the previous results. It was concluded that the combined administration of Quer and Mel may be useful as a potential therapy against renal injury induced by Sod ntr. HIF-1α and HSP-70 are implicated in the induction of hypoxia and its treatment.

scholarly journals CD40/CD40L contributes to hypercholesterolemia-induced microvascular inflammation

2009 ◽  
Vol 296 (3) ◽  
pp. H689-H697 ◽  
Author(s):  
Karen Y. Stokes ◽  
LeShanna Calahan ◽  
Candiss M. Hamric ◽  
Janice M. Russell ◽  
D. Neil Granger
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
T Cell ◽  
Blood Cell ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Microvascular Dysfunction ◽  
Cd40 Ligand ◽  
Scid Mice ◽  
Endothelial Cell Function

Hypercholesterolemia is associated with phenotypic changes in endothelial cell function that lead to a proinflammatory and prothrombogenic state in different segments of the microvasculature. CD40 ligand (CD40L) and its receptor CD40 are ubiquitously expressed and mediate inflammatory responses and platelet activation. The objective of this study was to determine whether CD40/CD40L, in particular T-cell CD40L, contributes to microvascular dysfunction induced by hypercholesterolemia. Intravital microscopy was used to quantify blood cell adhesion in cremasteric postcapillary venules, endothelium-dependent vasodilation responses in arterioles, and microvascular oxidative stress in wild-type (WT) C57BL/6, CD40-deficient (−/−), CD40L−/−, or severe combined immune deficient (SCID) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 wk. WT-HC mice exhibited an exaggerated leukocyte and platelet recruitment in venules and impaired vasodilation responses in arterioles compared with ND counterparts. A deficiency of CD40, CD40L, or lymphocytes attenuated these responses to HC. The HC phenotype was rescued in CD40L−/− and SCID mice by a transfer of WT T cells. Bone marrow chimeras revealed roles for both vascular- and blood cell-derived CD40 and CD40L in the HC-induced vascular responses. Hypercholesterolemia induced an oxidative stress in both arterioles and venules of WT mice, which was abrogated by either CD40 or CD40L deficiency. The transfer of WT T cells into CD40L−/− mice restored the oxidative stress. These results implicate CD40/CD40L interactions between circulating cells and the vascular wall in both the arteriolar and venular dysfunction elicited by hypercholesterolemia and identify T-cell-associated CD40L as a key mediator of these responses.

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

scholarly journals Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4210
Author(s):  
Yan Zhou ◽  
Chunxiu Zhou ◽  
Xutao Zhang ◽  
Chi Teng Vong ◽  
Yitao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Vascular Function ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Diabetic Mice ◽  
And Oxidative Stress

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

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