MOLECULAR BIOLOGY REPORTS
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2025
·Vol. 52
·期 1
·1-14
·
IF 2.8
Liang Chen,Guo Liping,Tian Xinyan,Mu Zhidan,Chen Mingyang,Hu Yarong,Su Juan
Objective By establishing a mouse model of hepatic ischemia–reperfusion injury (HIRI), to investigate the effects of cyclooxygenase-2 (COX-2) and endoplasmic reticulum stress (ERS) on HIRI and their interaction in HIRI. Methods C57BL/6J male mice were divided into four groups: Sham operation group (Sham group), hepatic ischemia–reperfusion (HIR) group, hepatic ischemia–reperfusion + Salubrinal (ER stress inhibitor) pretreatment group (HIR + Sal group), hepatic ischemia–reperfusion + NS398 (inhibitor of COX-2) pretreatment group (HIR + NS398 group). The levels of Aspartate transaminase (AST) and Alanine transaminase (ALT) in serum, the activity of Super Oxide Dismutase (SOD) and the content of malondialdehyde (MDA) in liver tissue were detected. The mRNA and protein expression of Glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), phosphorylated eukaryotic translation initiation factor 2α (p-eIF2α) and COX-2/PTGS (Prostaglandin-endoperoxide synthase) in liver tissue were detected. The morphological changes and apoptosis of liver tissue were observed. Results Compared with the Sham group, the serum ALT and AST levels of the HIR group were increased, the SOD activity in the liver tissue was decreased, the MDA content and the expression of COX-2, p-eIF2α, GRP78 and CHOP protein were increased, and the staining results showed that hepatic sinusoidal congestion, a large number of hepatocyte death, inflammatory cell infiltration and apoptotic cells were significantly increased. The levels of ALT and AST decreased after Sal or NS398 pretreatment. SOD activity was increased, MDA content, COX-2, GRP78, CHOP mRNA and protein were decreased in liver tissue, and staining showed that liver tissue injury was improved. Conclusion In mice with HIR, COX-2 interacts with ERS to cause liver injury by regulating oxidative stress and apoptosis.
研究领域:
分子生物学
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病理学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
Genes
·
2022
·Vol. 13
·期 11
·2133
·
IF 4.141
Jiahui Lin,Xianhui Lai,Xiaoxi Fan,Bozhi Ye,Lingfeng Zhong,Yucong Zhang,Ruiyin Shao,Si Shi,Weijian Huang,Lan Su,Miaomiao Ying
Pyroptosis serves a crucial function in various types of ischemia and reperfusion injuries. Oridonin, a tetracycline diterpene derived fromRabdosia rubescens, can significantly inhibit the aggregation of NLRP3-mediated inflammasome. This experiment is aimed at investigating the effect of oridonin on pyroptosis in mice cardiomyocytes. Based on the models of myocardial ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R), Evans Blue/TTC double staining, TUNEL staining, and Western blotting were applied to determine the effects of oridonin on myocardial damage, cellular activity and signaling pathways involved in pyroptosis. During I/R and H/R treatments, the extent of gasdermin D-N domains was upregulated in cardiomyocytes. Apart from that, oridonin improved cell survival in vitro and decreased the myocardial infarct size in vivo by also downregulating the activation of pyroptosis. Finally, the expression levels of ASC, NLRP3 and p-p65 were markedly upregulated in cardiomyocytes after H/R treatment, whereas oridonin suppressed the expression of these proteins. The present experiment revealed that myocardial I/R injury and pyroptosis can be alleviated and inhibited by oridonin pretreatment via NF-κB/NLRP3 signaling pathway, both in vivo and in vitro. Therefore, oridonin may serve as a potentially novel agent for the clinical treatment of myocardial ischemia-reperfusion injuries.Keywords:oridonin;cardiac ischemia/reperfusion injury;pyroptosis;GSDMD
研究领域:
心脏病学
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药理学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ELECTROCARDIOLOGY
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2017
·
IF 1.514
Yaoxu Chen,Chunxia Yin,Yingying Yang,Zhuo Fan,Jinling Shang,Wen Tan
Ischemia/reperfusion (I/R) induces prolongation of QT interval and action potential duration (APD), which is a major cardiac electrical disorder in patients with arrhythmias. However, the mechanism of QT interval prolongation induced by I/R remains unclear. In the present study, we hypothesized that the rapid component of delayed rectifier potassium ( I Kr ) channel plays an important role in I/R-induced QT interval prolongation. We observed a marked attenuation of I Kr and a significant prolongation of action potential duration (APD) in a simulated I/R system with sodium dithionite (Na 2 S 2 O 4 ) in ventricular myocytes of guinea pigs. The I Kr current density was inhibited by 64% and APD increased by 87% respectively. Moreover, the inhibition of I Kr is primarily ascribed to overproduction of reactive oxygen species (ROS) by I/R, which can be partly reversed by antioxidant vitamin E (100 μmol/L). The value of I Kr tail current density increased from 0.516 ± 0.040 pA/pF in I/R to 0.939 ± 0.091 pA/pF when treated with vitamin E. Moreover, we also demonstrated that QTc interval was increased by I/R and reversed by Vitamin E in isolated guinea pig hearts. In conclusion, the inhibition of I Kr is one of the underlying mechanisms of prolongation of QT interval and APD in I/R. Vitamin E might have a benefit in coronary reperfusion therapy .
研究领域:
心脏病学
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药理学
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生理学
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DOI
PubMed
高影响因子
Scientific Reports
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2025
·Vol. 15
·期 1
·1-14
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IF 3.9
Zhang Yuxi,Zhan Junbiao,Qiu Zhen,Tian Hao,Lei Shaoqing,Huang Qin,Xue Rui,Sun Qian,Xia Zhongyuan
Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in mitigating I/R injury. Meanwhile, verbascoside (VB), an active compound extracted from the herbaceous plant, has demonstrated myocardial protective effects. In this study, heart transplantation was performed using a modified non-suture cuff technique, with VB administered at a dose of 20 mg/kg/day via intraperitoneal injection for 3 days in vivo. In vitro, cardiomyocytes were pretreated with 50 µg/ml VB for 24 h. VB treatment significantly reduced histopathological injury, decreased myocardial injury markers, and inhibited ferroptosis and oxidative stress during myocardial cold I/R injury in vivo. In vitro experiments further demonstrated that GDF15 alleviates ferroptosis induced by hypoxic reoxygenation by upregulating GPX4. Therefore, it is concluded that VB preconditioning can effectively reduce ferroptosis induced by myocardial cold I/R after heterotopic heart transplantation, possibly through up-regulation of GDF15/GPX4/SLC7A11 pathway.
研究领域:
心血管病学
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药理学
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移植学
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DOI
PubMed
高影响因子
MOLECULAR NEUROBIOLOGY
·
2024
·
IF 4.6
Chen Kechun,Xu Bingtian,Long Lu,Wen Huizhen,Zhao Qian,Tu Xingxing,Wang Jiakang,Xu Jiangping,Wang Haitao
We have previously shown that inhibition of phosphodiesterase 4 (PDE4) protects against cerebral ischemia/reperfusion injury. However, it remains unclear whether and how PDE4 affects ferroptosis under cerebral ischemia/reperfusion conditions. In this study, we found that overexpression of PDE4B in HT-22 cells exacerbated the detrimental effects of oxygen–glucose deprivation/reoxygenation (OGD/R), including a decrease in cell viability and glutathione (GSH) levels and an increase in Fe 2+ content. PDE4B knockdown mitigated the effects of OGD/R, as evidenced by decreased oxidative stress, lactate dehydrogenase (LDH) release, Fe 2+ content, and nuclear receptor coactivator 4 (NCOA4) expression. PDE4B knockdown also enhanced the levels of GSH, ferroportin (FPN), and ferritin heavy chain 1 (FTH1). Consistently, inhibition of PDE4 by roflumilast (Roflu) produced similar effects as PDE4B knockdown. Roflu also ameliorated the morphology and membrane potential of the mitochondria. Glutathione peroxidase 4 (GPX4) knockdown blocked the effects of Roflu on cell viability and lipid peroxidation. Moreover, we found that nuclear factor erythroid 2-related factor 2 (Nrf-2) knockdown decreased GPX4 expression. In addition, Nrf-2 knockdown led to enhanced lipid peroxidation, LDH release, and iron levels, while the GSH and FPN levels decreased. More crucially, PDE4 inhibition decreased infarct volume, alleviated oxidative stress, and restored the expression levels of ferroptosis-associated proteins in middle cerebral artery occlusion/reperfusion (MCAO/R) rats. Interestingly, the GPX4 inhibitor RSL3 blocked the neuroprotective effects of Roflu in rats subjected to MCAO/R. Thus, PDE4 inhibition significantly inhibits neuronal ferroptosis by activating the Nrf-2/GPX4 pathway. These data indicate the existence of a novel mechanism underlying the neuroprotective effects of PDE4 inhibition.
研究领域:
神经科学
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药理学
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细胞生物学
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神经保护
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2020
·Vol. 47
·期 1
·302-314
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IF 3.098
Shu‑Jin Du,Ying Zhang,Yan‑Meng Zhao,Ya‑Jie Dong,Jing‑Long Tang,Xiao‑Hong Zhou,Wei‑Juan Gao
Cerebral ischemia‑reperfusion injury (CIRI), caused by the reperfusion of blocked vessels following ischemic stroke, can lead to secondary brain injury. Throughout CIRI, apoptosis serves an important role. Astragaloside IV is a potential neuroprotectant that alleviates CIRI by inhibiting apoptosis. The calcium‑sensing receptor (CaSR) is a G‑protein‑coupled receptor, the activation of which aggravates ischemia‑reperfusion injury. The aim of the present study was to investigate whether the protective effect of Astragaloside IV on CIRI may be associated with the regulation of CaSR. A rat middle cerebral artery occlusion/reperfusion (MCAO/R) model and an oxygen and glucose deprivation/reoxygenation (OGD/R) model of pheochromocytoma (PC12) cells were used to study the neuronal injury induced by CIRI. Neurological function scores (NFS), 2,3,5‑triphe‑nylterazolium chloride and hematoxylin and eosin staining were used to determine brain damage in rats. Cell viability was measured to evaluate the injury of OGD/R PC12 cells. Western blotting was used to examine the expression of proteins associated with apoptosis and CaSR. The CaSR antagonist NPS‑2143 and agonist GdCl3 were used to further confirm the effects of CaSR during the process of apoptosis. The results demonstrated that Astragaloside IV alleviated CIRI by decreasing the NFS of rats, reducing the infarction volume of the brain and promoting the viability of PC12 cells, as well as inhibiting the expression of cleaved caspase‑3 and CaSR, which was induced by CIRI. The results of the present study suggested that the activation of CaSR may be involved in CIRI‑induced brain damage in rats, and that Astragaloside IV may alleviate CIRI by inhibiting CaSR activation‑induced apoptosis.
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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DOI
PubMed
高影响因子
Food & Function
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2022
·Vol. 13
·期 13
·7062-7074
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IF 6.317
Fengwei Ma,Qingfang Deng,Huayong Lou,Jinyu Li,Su Xu,Wenneng Wu,Qihua Wen,Lei Tang,Xin Wang,Weidong Pan
Self-heal (Prunella vulgaris L.) is a perennial edible plant that is widely distributed across the world and is traditionally consumed as a food additive in soft drink beverages. In this study, to explore the functional components of P. vulgaris, an investigation of its ethanol extracts has been conducted by our group. As a result, twelve (1–12) vulgarisin-type diterpenoids with a special 5/6/4/5-fused ring skeleton, including six new ones (1–6), were obtained. Their structures including the absolute configuration were elucidated based on comprehensive spectroscopic evidence, ECD calculations, as well as single-crystal X-ray diffraction analyses. All the isolates were tested for neuroprotective effects against ischemia/reperfusion (I/R) on primary neuron cells through the oxygen and glucose deprivation and reperfusion (OGD/R) induced injury model. The results showed that all twelve vulgarisin-type diterpenoids possess promising neuroprotective activity at a concentration of 10 μM. Among them, compound 3 can significantly suppress cell apoptosis by regulating Bax/Bcl-2 protein expression and inhibiting cleaved caspase-3 and caspase-9 expression with a western blotting assay. Further research revealed that compound 3 could improve mitochondrial function by inhibiting mitochondrial cytochrome c release, reducing ROS levels, and maintaining the membrane potential. This work firstly reports vulgarisin-type diterpenoids possessing neuroprotective activity. These findings also suggest that daily consumption of P. vulgaris might prevent cerebral disorders via a mitochondria-related pathway.
研究领域:
药理学
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神经科学
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植物化学
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DOI
PubMed
高影响因子
INFLAMMATION
·
2018
·Vol. 41
·期 6
·2068-2078
·
IF 2.884
Zhou Qin,Gong Xia,Kuang Ge,Jiang Rong,Xie Tianjun,Tie HongTao,Chen XiaHong,Li Ke,Wan JingYuan,Wang Bin
Ferulic acid (FA), derived from fruits and vegetables, is well-known as a potent antioxidant of scavenging free radicals. However, the role and underlying mechanism of FA on kidney ischemia reperfusion (I/R) injury are limited. Here, we explored the effects of FA on kidney I/R injury. The kidney I/R injury models were carried out by clamping bilateral pedicles for 35 min followed by reperfusion for 24 h. Mice were orally pretreated with different doses of FA for three times 24 h before I/R. The renal function was assessed by serum creatine (Scr) and blood urea nitrogen (BUN). Kidney histology was examined by hematoxylin and eosin (HE) staining and terminal deoxynucleotidly transferased UTP nick-end labeling (TUNEL) assay. Proinflammatory cytokines, caspase-3 activity, adenosine generation, adenosine signaling molecules, and hypoxia inducible factor-1 alpha (HIF-1α) were also detected, respectively. The siHIF-1α adenovirus vectors were in vivo used to inhibit the expression of HIF-1α. The results showed that FA significantly attenuated kidney damage in renal I/R-operated mice as indicated by reducing levels of Scr and BUN, ameliorating renal pathological structural changes, and tubular cells apoptosis. Moreover, FA pretreatment inhibited I/R-induced renal proinflammatory cytokines and neutrophils recruitment. Interestingly, the levels of HIF-α, CD39, and CD73 mRNA and protein as well as adenosine production were all significantly increased after FA pretreatment in the kidney of I/R-performed mice, and inhibiting HIF-α expression using siRNA abolished this protection of FA on I/R-induced acute kidney injury as evidenced by more severe renal damage and reduced adenosine production. Our findings indicated that FA protected against kidney I/R injury by reducing apoptosis, alleviating inflammation, increasing adenosine generation, and upregulating CD39 and CD73 expression, which might be mediated by HIF-1α.
研究领域:
药理学
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分子生物学
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肾脏病学
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DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2024
·
IF 4.2
Dong-Jing Yang,Yang Bai,Min Wu,Yin-Ming Liang,Bin-Hui Zhou,Wenzhi Guo,Shui-Jun Zhang,Ji-Hua Shi
Vascular endothelial inflammation is crucial in hepatic ischemia–reperfusion injury (IRI). Our previous research has shown that connective tissue growth factor (CTGF), secreted by endothelial cells, protects against acute liver injury, but its upstream mechanism is unclear. We aimed to clarify the protective role of CTGF in endothelial cell inflammation during IRI and reveal the regulation between endoplasmic reticulum stress-induced activating transcription factor 6 (ATF6) and CTGF. Hypoxia/reoxygenation in endothelial cells, hepatic IRI in mice and clinical specimens were used to examine the relationships between CTGF and inflammatory factors and determine how ATF6 regulates CTGF and reduces damage. We found that activating ATF6 promoted CTGF expression and reduced liver damage in hepatic IRI. In vitro, activated ATF6 upregulated CTGF and downregulated inflammation, while ATF6 inhibition had the opposite effect. Dual-luciferase assays and chromatin immunoprecipitation confirmed that activated ATF6 binds to the CTGF promoter, enhancing its expression. Activated ATF6 increases CTGF and reduces extracellular regulated protein kinase 1/2 (ERK1/2) phosphorylation, decreasing inflammatory factors. Conversely, inhibiting ATF6 decreases CTGF and increases the phosphorylation of ERK1/2, increasing inflammatory factor levels. ERK1/2 inhibition reverses this effect. Clinical samples have shown that CTGF increases after IRI, inversely correlating with inflammatory cytokines. Therefore, ATF6 activation during liver IRI enhances CTGF expression and reduces endothelial inflammation via ERK1/2 inhibition, providing a novel target for diagnosing and treating liver IRI.
研究领域:
分子生物学
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肝病学
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炎症
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转录因子
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产品关联
DOI
PubMed
高影响因子
HEPATOLOGY
·
2024
·
IF 12.9
Zhang Sitong,Sun Zhongquan,Chen Zhenhua,Bi Yanli,Wei Shenyu,Mao Zhengwei,Jin Jin,Ding Yuan,Wang Weilin
Background & Aims: Liver ischemia-reperfusion injury (IRI) is a common complication of liver transplantation and hepatectomy, and causes acute liver dysfunction and even organ failure. Myeloid-derived suppressor cells (MDSCs) accumulate and play immunosuppressive function in cancers and inflammation. However, the role of MDSCs in liver IRI has not been defined. Approach & Results: We enrolled recipients receiving orthotopic liver transplantation (OLT) and obtained the pre-OLT/post-OLT blood and liver samples. The proportions of MDSCs were significantly elevated after OLT and negatively associated with liver damage. In single-cell RNA-sequencing analysis of liver samples during OLT, two cell clusters with MDSC-like phenotypes were identified and showed maturation and infiltration in post-OLT livers. In mice model, liver IRI mobilized MDSCs and promoted their infiltration in damaged liver, and intrahepatic MDSCs possessed with enhanced immunosuppressive function by up-regulation of STAT3 signaling. Under treatment with αGr-1 antibody or adoptive transfer MDSCs to change the proportion of MDSCs in vivo , we found that intrahepatic MDSCs alleviated liver IRI-induced inflammation and damage by inhibiting M1 macrophage polarization. Mechanistically, bulk RNA-sequencing analysis and in vivo experiments verified that CXCL17 was upregulated by YAP/TEAD1 signaling and subsequently recruited MDSCs via binding with GPR35 during liver IRI. Moreover, hepatic endothelial cells were the major cells responsible for CXCL17 expression in injured livers, among which hypoxia-reoxygenation stimulation activated YAP/TEAD1 complex to promote CXCL17 transcription. Conclusions: Endothelial YAP/TEAD1-CXCL17 signaling recruited MDSCs to attenuate liver IRI, providing evidence of a therapeutic potential for managing IRI in liver surgery. Export
研究领域:
医学
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免疫学
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肝脏病学
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
·
IF 4.7
Kun Zhang,Kehui Yang,Lingyuan Zeng,Yang Xiao,JinGui Yu
Myocardial cell injury resulting from myocardial ischemia and reperfusion is one of the primary drivers behind the onset and progression of heart disease. Penehyclidine hydrochloride (PHC), a novel selective anti-cholinergic agent, exerts a protective effect against myocardial ischemia-reperfusion injury (MIRI). Rab32 belongs to the family of small GTPase proteins. The present study aimed to investigate whether PHC improved MIRI by regulating Rab32 and to explore the underlying mechanisms. Oxygen-glucose deprivation/reoxygenation (OGD/R) and left anterior descending coronary artery ligation were used to establish MIRI models in vitro and in vivo. Here, we showed that PHC upregulated the expression of Rab32 in OGD/R treated HL-1 cells. PHC alleviated OGD/R-induced cell apoptosis and intracellular and mitochondrial ROS levels, while the downregulation of Rab32 exacerbated cell injury. Rab32 was upregulated in MIRI mice and downregulated in OGD/R-induced HL-1 cells. Rab32 overexpression improved cardiac function, reduced the myocardial infarct size, and inhibited cell apoptosis and mitochondrial dysfunction, either in MIRI mice or OGD/R-induced HL-1 cells. On the mechanism, Rab32 interacted with Fancd2 in HL-1 cells. Rab32 downregulation decreased Fancd2 protein expression in mitochondria. Rab32 anchored Fancd2 to mitochondria in OGD/R treated HL-1 cells. Fancd2 knockdown reversed the protective effect of Rab32 on OGD/R-induced HL-1 cells and aggravated cardiomyocyte injury. Finally, the protective role of PHC on MIRI-caused cardiomyocyte injury was confirmed in MIRI mice. Overall, we demonstrated that Rab32 protects mitochondrial function by anchoring Fancd2 and mediates the protective effect of PHC against MIRI.
研究领域:
心血管病学
·
细胞生物学
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分子医学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2024
·
IF 4.8
Luyao Liu,Ruikun Wang,Weijuan Gao,Xianming Hou,Xiaofei Jin,Yanmeng Zhao,Xiaohong Zhou,Yi Zhang
Ethnopharmacological relevance Cerebral ischemia-reperfusion (I/R) injury is a common complication of ischemic stroke, with autophagy and pyroptosis playing key roles. Huangqi and Danggui (HQDG) are a commonly used drug pair of Chinese traditional medicine for clinical treatment of ischemic stroke. Aim of the study The study aims to investigate the interaction between autophagy and pyroptosis regulated by HQDG through the AMPK/mTOR signaling pathway during cerebral I/R injury. Materials and methods Model of middle-cerebral artery occlusion/reperfusion (MCAO/R) in SD rats was established using the Longa suture method. The components of traditional Chinese medicine were detected by liquid chromatography coupled to quadrupole orbitrap high resolution mass spectrometry (LC/MS). Neurological deficits were evaluated by neurological function score. Changes of cerebral blood flow were detected by a laser speckle blood flow imaging instrument. The volume of cerebral infarction was observed by 2,3,5-Chlorotriphenyltetrazolium (TTC) staining. The permeability of the blood-brain barrier was measured by Evans blue test. Neurovascular unit and autophagosomes in brain tissue were assessed by transmission electron microscopy. Neuronal pyroptosis was detected by terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL)/Caspase-1 staining. The expression of autophagy related proteins, pyroptosis related proteins, and AMPK/mTOR pathway related proteins were detected by Western blot. Results After cerebral I/R injury, autophagy and pyroptosis, were characterized by increased number of autophagosomes and pyroptosis cells, upregulated expression of Beclin 1, LC3-II/LC3-I, NLRP3, cleaved Caspase-1, IL-1beta, IL-18 proteins, and downregulated expression of P62 proteins. HQDG significantly improved neurological function, reduced the volume of cerebral infarction, increased cerebral blood flow, improved blood-brain barrier permeability and the function of neurovascular units. Autophagy was further activated and pyroptosis was significantly inhibited by HQDG, which promoted increased number of autophagosomes, enhanced expression of Beclin 1, LC3-II/LC3-I proteins, reduced expression of P62, NLRP3, cleaved Caspase-1, IL-1beta, and IL-18 proteins, and downregulated the number of pyroptosis cells. On the other hand, after administering 3-Methyladenine (3-MA) to inhibit autophagy, the above effects of HQDG were significantly inhibited. Besides, HQDG promoted AMPK phosphorylation, and weakened mTOR phosphorylation. However, after the administration of AMPK inhibitor Compound C, HQDG caused increase in Beclin 1 and LC3-II/LC3-I, reduced P62 and NLRP3, and cleaved Caspase-1 protein expression, whereas cerebral blood flow decreased. Conclusion HQDG alleviated pyroptosis by promoting autophagy via AMPK/mTOR signaling pathway after middle-cerebral artery occlusion/reperfusion in rats, showing its potential for treatment of cerebral I/R injury in humans.
研究领域:
药理学
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神经科学
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中医药
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分子生物学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）