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Biochanin A attenuates spinal cord injury in rats during early stages by inhibiting oxidative stress and inflammasome activation

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Neural Regeneration Research 2024年第9期19卷 2050-2056页

作者： Xigong Li Jing Fu Ming Guan Haifei Shi Wenming Pan Xianfeng Lou Department of Orthopedics The First Affiliated Hospital of Zhejiang UniversityHangzhouZhejiang ProvinceChina Department of Stomatology Xixi HospitalHangzhouZhejiang ProvinceChina Department of Orthopedics and Spine Surgerythe Affiliated Hospital of Xuzhou Medical Schoolthe Second People’s Hospital of ChangshuChangshuJiangsu ProvinceChina

Previous studies have shown that Biochanin A,a flavonoid compound with estrogenic effects,can serve as a neuroprotective agent in the context of cerebral ischemia/reperfusion injury;howeve r,its effect on spinal cord injury is still unclea r. In this study,a rat model of spinal cord injury was established using the heavy o bject impact method,and the rats were then treated with Biochanin A(40 mg/kg) via intrape ritoneal injection for 14 consecutive days.The res ults showed that Biochanin A effectively alleviated spinal cord neuronal injury and spinal co rd tissue injury,reduced inflammation and oxidative stress in spinal cord neuro ns,and reduced apoptosis and pyroptosis.In addition,Biochanin A inhibited the expression of inflammasome-related proteins(ASC,NLRP3,and GSDMD)and the Toll-like receptor 4/nuclear factor-κB pathway,activated the Nrf2/heme oxygenase 1 signaling pathway,and increased the expression of the autophagy markers LC3 Ⅱ,Beclin-1,and P62.Moreove r,the therapeutic effects of Biochanin A on early post-s pinal cord injury were similar to those of methylprednisolone.These findings suggest that Biochanin A protected neurons in the injured spinal cord through the Toll-like receptor 4/nuclear factor κB and Nrf2/heme oxygenase 1 signaling pathways.These findings suggest that Biochanin A can alleviate post-spinal cord injury at an early stage.

关键词： apoptosis autophagy Biochanin A heme oxygenase 1 inflammation Nrf2 protein nuclear factor kappa-B oxidative stress spinal cord injury Toll-like receptor 4

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Chinese herbal medicine compound Yi-Zhi-Hao pellet inhibits replication of influenza virus infection through activation of heme oxygenase-1

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Acta Pharmaceutica Sinica B 2017年第6期7卷 630-637页

作者： Jinqiu Yin Linlin Ma Huiqiang Wang Haiyan Yan Jin Hu Wen Jiang Yuhuan Li Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences and Peking Union Medical College School of Medical Technology Shanghai University of Medicine and Health Sciences Department of Pharmacy The Sixth Affiliated Hospital of Xinjiang Medical University

As a leading cause of respiratory disease, influenza A virus(IAV) presents a pandemic threat in annual seasonal outbreaks. Given the limitation of existing anti-influenza therapies, there remains to be a requirement for new drugs. Compound Yi-Zhi-Hao pellet(CYZH) is a famous traditional Chinese medicine(TCM) used in the clinic, whose formula has been recorded in Complication of National Standard for Traditional Chinese Medicine to treat common cold. In this study, we found that CYZH exhibited a broad-spectrum anti-influenza activity and inhibited the expression of viral RNA and proteins in vitro. Mechanistically, CYZH had no inhibitory activities against viral protein hemagglutinin and IAV RNA-dependent RNA polymerase. Instead, it induced activation of erythroid 2-related factor 2(Nrf2) and nuclear factor kappa B(NF-κB), which subsequently upregulated heme oxygenase-1(HO-1) expression.Also, CYZH protected cells from oxidative damage induced by reactive oxygen series. In conclusions,CYZH inhibits IAV replication in vitro, at least partly by activating expression of the Nrf2/HO-1 pathway.

关键词： TMC Influenza A virus heme oxygenase 1 Hemagglutinin Nrf2 NF-κB

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Rosmarinic acid elicits neuroprotection in ischemic stroke via Nrf2 and heme oxygenase 1 signaling

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Neural Regeneration Research 2018年第12期13卷 2119-2128页

作者： Hai-Ying Cui Xiang-Jian Zhang Yi Yang Cong Zhang Chun-Hua Zhu Jiang-Yong Miao Rong Chen Department of Neurology Second Hospital of hebei Medical university Shijiazhuang Hebei Province China Hebei Key Laboratory of Vascular Homeostasis and Hebei Collaborative Innovation Center for Cardiocerebrovascular Disease ShijiazhuangHebei Province China

Rosmarinic acid（RA） can elicit a neuroprotective effect against ischemic stroke, but the precise molecular mechanism remains poorly understood. In this study, an experimental ischemic stroke model was established in CD-1 mice（Beijing Vital River Laboratory Animal Technology, Beijing, China） by occluding the right middle cerebral artery for 1 hour and allowing reperfusion for 24 hours. After intraperitoneally injecting model mice with 10, 20, or 40 mg/kg RA, functional neurological deficits were evaluated using modified Longa scores. Subsequently, cerebral infarct volume was measured using TTC staining and ischemic brain tissue was examined for cell apoptosis with TUNEL staining. Superoxide dismutase activity and malondialdehyde levels were measured by spectrophometry. Expression of heme oxygenase-1（HO-1）, nuclear factor erythroid 2-related factor 2（Nrf2）, Bcl-2, Bax, Akt, and phospho-Ser473 Akt proteins in ischemic brain tissue was detected by western blot, while mRNA levels of Nrf2, HO-1, Bcl-2, and Bax were analyzed using real time quantitative PCR. In addition, HO-1 enzyme activity was measured spectrophotometrically. RA（20 and 40 mg/kg） greatly improved neurological function, reduced infarct volume, decreased cell apoptosis, upregulated Bcl-2 protein and mRNA expression, downregulated Bax protein and mRNA expression, increased HO-1 and Nrf2 protein and mRNA expression, increased superoxide dismutase activity, and decreased malondialdehyde levels in ischemic brain tissue of model mice. However, intraperitoneal injection of a HO-1 inhibitor（10 mg/kg zinc protoporphyrin IX） reversed the neuroprotective effects of RA on HO-1 enzyme activity and Bcl-2 and Bax protein expression. The PI3 K/Akt signaling pathway inhibitor LY294002（10 mM） inhibited Akt phosphorylation, as well as Nrf2 and HO-1 expression. Our findings suggest that RA has anti-oxidative and anti-apoptotic properties that protect against ischemic stroke by a mechanism involving upregulation of Nrf2 and HO-1 expression via the PI3 K/Akt signaling pathwa

关键词： cerebral ischemia/reperfusion rosmarinic acid cellular apoptosis oxidative injury neuroprotection Bcl-2 Bax Nrf2 heme oxygenase 1 PI3K/Akt signal pathway neural regeneration

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Upregulation of CDGSH iron sulfur domain 2 attenuates cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2023年第7期18卷 1512-1520页

作者： Miao Hu Jie Huang Lei Chen Xiao-Rong Sun Zi-Meng Yao Xu-Hui Tong Wen-Jing Jin Yu-Xin Zhang Shu-Ying Dong Department of Pharmacology School of PharmacyBengbu Medical CollegeBengbuAnhui ProvinceChina Key Laboratory of Cardiovascular and Cerebrovascular Diseases Bengbu Medical CollegeBengbuAnhui ProvinceChina Anhui Engineering Technology Research Center of Biochemical Pharmaceutical BengbuAnhui ProvinceChina

CDGSH iron sulfur domain 2 can inhibit ferroptosis,which has been associated with cerebral ischemia/reperfusion,in individuals with head and neck cancer.Therefore,CDGSH iron sulfur domain 2 may be implicated in cerebral ischemia/reperfusion injury.To validate this hypothesis in the present study,we established mouse models of occlusion of the middle cerebral artery and HT22 cell models of oxygen-glucose deprivation and reoxygenation to mimic cerebral ischemia/reperfusion injury in vivo and in vitro,respectively.We found remarkably decreased CDGSH iron sulfur domain 2 expression in the mouse brain tissue and HT22 cells.When we used adeno-associated virus and plasmid to up-regulate CDGSH iron sulfur domain 2 expression in the brain tissue and HT22 cell models separately,mouse neurological dysfunction was greatly improved;the cerebral infarct volume was reduced;the survival rate of HT22 cells was increased;HT22 cell injury was alleviated;the expression of ferroptosis-related glutathione peroxidase 4,cystine-glutamate antiporter,and glutathione was increased;the levels of malondialdehyde,iron ions,and the expression of transferrin receptor 1 were decreased;and the expression of nuclear-factor E2-related factor 2/heme oxygenase 1 was increased.Inhibition of CDGSH iron sulfur domain 2 upregulation via the nuclear-factor E2-related factor 2 inhibitor ML385 in oxygen-glucose deprived and reoxygenated HT22 cells blocked the neuroprotective effects of CDGSH iron sulfur domain 2 up-regulation and the activation of the nuclear-factor E2-related factor 2/heme oxygenase 1 pathway.Our data indicate that the up-regulation of CDGSH iron sulfur domain 2 can attenuate cerebral ischemia/reperfusion injury,thus providing theoretical support from the perspectives of cytology and experimental zoology for the use of this protein as a therapeutic target in patients with cerebral ischemia/reperfusion injury.

关键词： cerebral ischemia/reperfusion injury CDGSH iron sulfur domain 2 ferroptosis glutathione peroxidase 4 heme oxygenase 1 HT22 nuclear-factor E2-related factor 2 oxygen-glucose deprivation/reoxygenation injury stroke transferrin receptor 1

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Region-dependent effects of diabetes and insulin-replacement on neuronal nitric oxide synthase-and heme oxygenase-immunoreactive submucous neurons

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World Journal of Gastroenterology 2017年第41期23卷 7359-7368页

作者： Nikolett Bódi Zita Szalai Lalitha Chandrakumar Mária Bagyánszki Department of Physiology Anatomy and Neuro-science Faculty of Science and Informatics University of Szeged

AIM To investigate the intestinal segment-specific effects of diabetes and insulin replacement on the density of different subpopulations of submucous neurons. METHODS Ten weeks after the onset of type 1 diabetes samples were taken from the duodenum, ileum and colon of streptozotocin-induce diabetic, insulin-treated diabetic and sex-and age-matched control rats. Whole-mount preparations of submucous plexus were prepared from the different gut segments for quantitative fluorescent immunohistochemistry. The following double-immunostainings were performed: neuronal nitric oxide synthase(n NOS) and Hu C/D, heme oxygenase(HO) 1 and peripherin, as well as HO2 and peripherin. The density of n NOS-, HO1-and HO2-immunoreactive(IR) neurons was determined as a percentage of the total number of submucous neurons. RESULTS The total number of submucous neurons and the proportion of n NOS-, HO1-and HO2-IR subpopulations were not affected in the duodenal ganglia of control, diabetic and insulin-treated rats. While the total neuronal number did not change in either the ileum or the colon, the density of nitrergic neurons exhibited a 2-and 3-fold increase in the diabetic ileum and colon, respectively, which was further enhanced after insulin replacement. The presence of HO1-and HO2-IR submucous neurons was robust in the colon of controls(38.4%-50.8%), whereas it was significantly lower in the small intestinal segments(0.0%-4.2%, P < 0.0001). Under pathophysiological conditions the only alteration detected was an increase in the ileum and a decrease in the colon of the proportion of HO-IR neurons in insulin-treated diabetic animals. CONCLUSION Diabetes and immediate insulin replacement induce the most pronounced region-specific alterations of n NOS-, HO1-and HO2-IR submucous neuronal density in the distal parts of the gut.

关键词： Nitrergic neurons heme oxygenase 1 heme oxygenase 2 Submucous neurons Gut regionspecificity Diabetes Insulin

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A ferroptosis-inducing iridium(III) complex

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Science China Chemistry 2020年第1期63卷 65-72页

作者： Xiuxiu Wang Feng Chen Jingyi Zhang Jianxuan Sun Xinyang Zhao Yuelu Zhu Wei Wei Jing Zhao Zijian Guo State Key Laboratory of Coordination Chemistry Institute of Chemistry and Biomedical SciencesSchool of Life SciencesNanjing UniversityNanjing 210023China School of Chemistry and Chemical Engineering Nanjing UniversityNanjing 210093China

Ferroptosis is a recently emerging non-apoptotic mode of cell death involving the production of iron-dependent reactive oxygen species(ROS).Here we described a mitochondria-targeted iridium(III)complex Ir FN that exhibited potent antiproliferative activity against a variety of cancer cells,especially the A2780 human ovarian cancer cells,through the ferroptosis pathways.Mechanistic studies by label-free quantitative proteomics profiling indicated that heme oxygenase 1(HMOX1)-mediated ferroptosis process was activated by Ir FN.The study on iron-dependent cell death,ROS accumulation,lipid peroxidation,and over released iron further confirmed the ferroptosis processes.m RNA transcription quantification,in vitro over-expression of HMOX1,and RNAi-mediated knock-down experiments suggested that Ir FN activated the over-expression of HMOX1.Our report revealed the first case of anticancer iridium complex leading to ferroptosis,highlighting ferroptosis as a promising approach in future design of metallodrugs.

关键词： iridium proteome ferroptosis heme oxygenase 1

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Protoporphyrin Treatment Modulates Susceptibility to Experimental Autoimmune Encephalomyelitis in MiR-155-deficient mice

Protoporphyrin Treatment Modulates Susceptibility to Experim...

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第十届全国免疫学学术大会

作者： Jinyu Zhang Michel Braun National Engineering Research Center of Immunological Products Department of Microbiology and Biochemical Pharmacy College of Pharmacy Third Military Medical University Institute for Medical Immunology Faculty of Medicine Université Libre de Bruxelles (ULB)

Background:Mi R-155 was shown to be critical for T cell fitness and effector functions.We previously identified heme oxygenase 1(HO-1)as a specific target of mi R-155,and inhibition of HO-1 activity restored the capacity of mi R-155-/-CD4+T cells to promote antigen-driven inflammation after adoptive transfer in antigen-expressing recipients.We questioned whether this observation could be extended to other systems where mi R-155 was shown to control the activity of chronically-stimulated T cells.The regulatory role played by mi R-155 on T cell-mediated chronic inflammation is well established in experimental autoimmune encephalomyelitis(EAE)model.In EAE,mi R-155 was up-regulated upon MOG35-55 immunization,and mi R-155-deficient mice were resistant to EAE.Protoporphyrins are molecules recognized for their modulatory effect on HO-1 expression and function.Aims:Investigate whether the resistance of mi R-155-/-mice to EAE could be lifted by the inhibition of HO-1.Methods:EAE was induced in mi R-155+/+and mi R-155-/-mice that received HO-1 activator Co PP,inhibitor Zn PP or vehicle alone.Flow cytometry was used to determine cellularity in spleen,lymph node and brain.Results:Induction of HO-1 by Co PP injection attenuated clinical signs of EAE in mi R-155+/+mice,while Zn PP treatment worsened clinical signs in mi R-155-/-mice.Lack of mi R-155 expression caused an important drop in the number of CD11b+cells,CD3+cells and B220+cells present within the brain.Inhibition of HO-1 by Zn PP,however,restored brain cellular infiltrates in mi R-155-/-mice to numbers comparable to those observed in wild type counterparts.Moreover,both the numbers of Th1 and Th17 cells present in the spleen,lymph node or brain of mi R-155-/-mice treated with Zn PP were very similar to those in vehicle-treated mi R-155+/+mice.Conclusion:Our work has confirmed the importance of mi R-155 in T cells for inhibiting HO-1 expression and promoting T cell-driven inflammation leading to autoimmune disease.

关键词： autoimmunity micro RNA heme oxygenase 1

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