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Metformin alleviates spinal cord injury by inhibiting nerve cell ferroptosis through upregulation of heme oxygenase-1 expression

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Neural Regeneration Research 2024年第9期19卷 2041-2049页

作者： Zhihua Wang Wu Zhou Zhixiong Zhang Lulu Zhang Meihua Li department of Neurosurgery The First Affiliated Hospital of Nanchang UniversityNanchangJiangxi ProvinceChina Postdoctoral Innovation Practice base The First Affiliated Hospital of Nanchang UniversityNanchangJiangxi ProvinceChina department of Nephrology Nanchang People’s Hospital Affiliated to Nanchang Medical CollegeNanchangJiangxi ProvinceChina

Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox homeostasis.Metformin is a classic drug used to treat type 2 diabetes that can inhibit ferroptosis.Previous studies have shown that,when used to treat cardiovascular and digestive system diseases,metformin can also upregulate heme oxygenase-1 expression.Therefore,we hypothesized that heme oxygenase-1 plays a significant role in mediating the beneficial effects of metformin on neuronal ferroptosis after spinal cord injury.To test this,we first performed a bioinformatics analysis based on the GEO database and found that heme oxygenase-1 was upregulated in the lesion of rats with spinal cord injury.Next,we confirmed this finding in a rat model of T9 spinal cord compression injury that exhibited spinal cord nerve cell ferroptosis.Continuous intraperitoneal injection of metformin for 14 days was found to both upregulate heme oxygenase-1 expression and reduce neuronal ferroptosis in rats with spinal cord injury.Subsequently,we used a lentivirus vector to knock down heme oxygenase-1 expression in the spinal cord,and found that this significantly reduced the effect of metformin on ferroptosis after spinal cord injury.Taken together,these findings suggest that metformin inhibits neuronal ferroptosis after spinal cord injury,and that this effect is partially dependent on upregulation of heme oxygenase-1.

关键词： acyl-CoA synthetase long-chain family member 4 ferroptosis glutathione peroxidase 4 heme oxygenase-1 inflammation iron lipid peroxidation metformin neuroprotection spinal cord injury

Plant-derived nanovesicles as an emerging platform for cancer therapy

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Acta Pharmaceutica Sinica B 2024年第1期14卷 133-154页

作者： Hanzhe Liu Guo-Feng Luo Zhengjun Shang The State Key Laboratory Breeding base of Basic Science of Stomatology(Hubei-MOST)&Key Laboratory of Oral Biomedicine Ministry of Education School and Hospital of StomatologyWuhan UniversityWuhan 430079China

Plant-derived nanovesicles(PDNVs)derived from natural green products have emerged as an attractive nanoplatform in biomedical application.They are usually characterized by unique structural and biological functions,such as the bioactive lipids/proteins/nucleic acids as therapeutics and targeting groups,immune-modulation,and long-term circulation.With the rapid development of nanotechnology,materials,and synthetic chemistry,PDNVs can be engineered with multiple functions for efficient drug delivery and specific killing of diseased cells,which represent an innovative biomaterial with high biocompatibility for fighting against cancer.In this review,we provide an overview of the state-of-theart studies concerning the development of PDNVs for cancer therapy.The original sources,methods for obtaining PDNVs,composition and structure are introduced systematically.With an emphasis on the featured application,the inherent anticancer properties of PDNVs as well as the strategies in constructing multifunctional PDNVs-based nanomaterials will be discussed in detail.Finally,some scientific issues and technical challenges of PDNVs as promising options in improving anticancer therapy will be discussed,which are expected to promote the further development of PDNVs in clinical translation.

关键词： Naturally occurring nanovesicles Plant Nanotechnology Drug delivery Cancer therapy

Malvidin Mitigates Sepsis-induced Cardiac Injury by Modulating the TLR4-iNOS-COX-2 Inflammatory Pathway and the Bax/Bcl-2/Cyto-C Mitochondrial Apoptosis Pathway in a p38 MAPK-dependent Manner

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Biomedical and Environmental Sciences 2024年第2期37卷 221-227页

作者： ZHANG Wei YUAN Si Long QIANG Jing Chao HUANG He LI Da SUN Ying ZHANG Hong Gang department of Vascular Surgery The First People’s Hospital of LianyungangLianyungang 222005JiangsuChina Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening College of PharmacyJiangsu Ocean UniversityLianyungang 222005JiangsuChina Jinzhou Medical University postgraduate training base(Lianyungang First People’s hospital) Lianyungang 222005JiangsuChina

In critical care medicine,sepsis is a dangerous systemic condition that is highly prevalent and is associated with high morbidity and mortality rates^([1]).The high mortality rate associated with sepsis is closely related to multi-organ dysfunction,with heart injury being particularly critical and considered the starting point of multi-organ injury^([2]).

关键词： mortality Apoptosis TLR4

Argatroban promotes recovery of spinal cord injury by inhibiting the PAR1/JAK2/STAT3 signaling pathway

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Neural Regeneration Research 2024年第2期19卷 434-439页

作者： Chenxi Zhao Tiangang Zhou Ming Li Jie Liu Xiaoqing Zhao Yilin Pang Xinjie Liu Jiawei Zhang Lei Ma Wenxiang Li Xue Yao Shiqing Feng department of Orthopedics Tianjin Medical University General HospitalTianjinChina International Science and Technology Cooperation base of Spinal Cord Injury Tianjin Key Laboratory of Spine and Spinal Cord InjuryDepartment of OrthopedicsTianjin Medical University General HospitalTianjinChina Orthopedic Research Center of Shandong University Cheeloo College of MedicineDepartment of OrthopedicsQilu Hospital of Shandong UniversityJinanShandong ProvinceChina

Argatroban is a synthetic thrombin inhibitor approved by U.S.Food and Drug Administration for the treatment of thrombosis.However,whether it plays a role in the repair of spinal cord injury is unknown.In this study,we established a rat model of T10 moderate spinal cord injury using an NYU Impactor ModerⅢand performed intraperitoneal injection of argatroban for 3 consecutive days.Our results showed that argatroban effectively promoted neurological function recovery after spinal cord injury and decreased thrombin expression and activity in the local injured spinal cord.RNA sequencing transcriptomic analysis revealed that the differentially expressed genes in the argatroban-treated group were enriched in the JAK2/STAT3 pathway,which is involved in astrogliosis and glial scar formation.Western blotting and immunofluorescence results showed that argatroban downregulated the expression of the thrombin receptor PAR1 in the injured spinal cord and the JAK2/STAT3 signal pathway.Argatroban also inhibited the activation and proliferation of astrocytes and reduced glial scar formation in the spinal cord.Taken together,these findings suggest that argatroban may inhibit astrogliosis by inhibiting the thrombin-mediated PAR1/JAK2/STAT3 signal pathway,thereby promoting the recovery of neurological function after spinal cord injury.

关键词： argatroban astrogliosis JAK/STAT signaling pathway protease-activated receptor-1 spinal cord injury thrombin vimentin

Is reactive oxygen species the only way for cancer inhibition over single atom nanomedicine?Autophagy regulation also works

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Chinese Chemical Letters 2024年第6期35卷 474-479页

作者： Yuanyi Zhou Ke Ma Jinfeng Liu Zirun Zheng Bo Hu Yu Meng Zhizhong Li Mingshan Zhu Postdoctoral Innovation Practice base The First and Fifth Affiliated Hospital of Jinan UniversityGuangzhou 510632China Guangdong Provincial Key Laboratory of Spine and Spinal Cord Reconstruction The Fifth Affiliated Hospital of Jinan University(Heyuan Shenhe People’s Hospital)Heyuan 517465China School of Environment Jinan UniversityGuangzhou 511443China department of Nephrology The First Affiliated Hospital of Jinan UniversityGuangzhou 510632China

Exploring the therapeutic effect of single atom catalysts beyond reactive oxygen species(ROS)modulation would boost the prosperity of nanomedicine in cancer treatment.Autophagy as a vital therapy target offers new options for the control of renal cell carcinoma(RCC)progression.Herein,Fe single atom-decorated graphene oxide(Fe_(1)-GO)nanosheet is developed to be a feasible autophagy inducer in RCC treatment.With the well-dispersed O-Fe_(1)-O active sites,Fe_(1)-GO kills ACHN cells effectively but maintains acceptable cytotoxicity to the normal podocyte and HK2 ones.In-depth analyses ascribe the inhibition of ACHN cells to the upregulated autophagy instead of the commonly known catalytic ROS generation.The in vivo therapeutic effect of Fe_(1)-GO nanomedicine is also validated by the RCC-bearing BALB/c mice model,realizing an 89% reduction of tumor weight and good biosafety.This work provides new insights into the design of autophagy regulators as well as potential therapeutic strategies for RCC treatment.

关键词： Fe single atom Autophagy Renal cell carcinoma Graphene oxide Cancer therapy

Exploring the molecular mechanisms and potential therapeutic strategies of ferroptosis in ovarian cancer

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BIOCELL 2024年第3期48卷 379-386页

作者： LISHA MA WANQI SHAO WEILI ZHU department of Gynecology Jiaxing University Master Degree Cultivation BaseZhejiang Chinese Medical UniversityJiaxingChina department of Gynecology Jiaxing University Affiliated Women and Children’s HospitalJiaxingChina

The morbidity rate of ovarian cancer,a malignant tumour in gynaecological tumours,is rising,and it is considered to be the most lethal cancer.The majority of patients are typically diagnosed during the advanced stages of the illness due to the elusive characteristics of ovarian cancer and an absence of highly sensitive and speciﬁc diagnostic indicators.Surgical excision of the lesions,along with chemotherapy,is the conventional treatment for ovarian cancer;however,resistance to platinum-based chemotherapeutic drugs and molecular targeted therapies frequently arises.Improving the survival rate and prognosis of patients with end-stage or recurring ovarian cancer requires the identiﬁcation of new therapeutic targets due to the absence of efﬁcient medications,and this has emerged as a highly demanding issue.Studies have demonstrated that ferroptosis effectively hinders the proliferation of ovarian cancer and induces the demise of malignant cells.Ferroptosis is composed of the cystine/glutamate antiporter system(the system Xc-)and glutathione peroxidase 4(GPX4).Solute carrier family 7 member 11(SLC7A11)and solute carrier family 3 member 2(SLC3A2)play crucial roles in the regulation of ferroptosis by facilitating the uptake of cystine into cells and the efﬂux of glutamate out of cells,respectively.In cells,GPX4 is the exclusive enzyme employed for reducing liposomal peroxide through glutathione peroxidase activity.The occurrence of ferroptosis in ovarian cancer is strongly associated with three main pathways,namely,the GPX4-glutathione(GSH)protective pathway,the ferroptosis suppressor protein 1(FSP1)-coenzyme Q10(CoQ10)protective pathway,and the guanosine 5'-triphosphate cyclohydrolase I(GCH1)protective pathway.In ovarian cancer cells,the postsynaptic density-95,discs-large,zona occludens 1(PDZ)-binding motif-angiopoietin-like 4-nicotinamide adenine dinucleotide phosphate oxidases 2(TAZ-ANGPTL4-NOX2)pathway can be regulated by Yes-associated protein(YAP)/TAZ,a downstream component of the Hippo pathway,leading to the mo

关键词： Ovarian cancer Ferroptosis Therapy

Single-cell RNA sequencing in juvenile idiopathic arthritis

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Genes & Diseases 2024年第2期11卷 633-644页

作者： Xiwen Luo Xuemei Tang department of Rheumatology and Immunology Children’s Hospital of Chongqing Medical UniversityChongqing 400014China Chongqing Key Laboratory of Child Infection and Immunity Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChildren's Hospital of Chongqing Medical UniversityChongqing 400014China

Juvenile idiopathic arthritis (JIA) is one of the most common chronic inflammatory rheumatic diseases in children,with onset before age 16 and lasting for more than 6 weeks.JIA is a highly heterogeneous condition with various consequences for health and quality of life.For some JIA patients,early detection and intervention remain challenging.As a result,further investigation of the complex and unknown mechanisms underlying JIA is required.Advances in technology now allow us to describe the biological heterogeneity and function of individual cell populations in JIA.Through this review,we hope to provide novel ideas and potential targets for the diagnosis and treatment of JIA by summarizing the current findings of single-cell RNA sequencing studies and understanding how the major cell subsets drive JIA pathogenesis.

关键词： Juvenile idiopathic arthritis Macrophage Macrophage activation syndrome Monocyte Single-cell RNA sequencing Synoviocyte T cell

Study on sex differences and potential clinical value of threedimensional computerized tomography pelvimetry in rectal cancer patients

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World Journal of Gastrointestinal Oncology 2024年第3期16卷 773-786页

作者： Xiao-Cong Zhou Fei-Yue Ke Gaurav Dhamija Hao Chen Qiang Wang department of Colorectal Surgery The Dingli Clinical Institute of Wenzhou Medical University(Wenzhou Central Hospital)Wenzhou 325000Zhejiang ProvinceChina Postgraduate Training base Alliance of Wenzhou Medical University Wenzhou Central HospitalWenzhou 325000Zhejiang ProvinceChina School of International Studies Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina department of Radiology The Dingli Clinical Institute of Wenzhou Medical University(Wenzhou Central Hospital)Wenzhou 325000Zhejiang ProvinceChina

BACKGROUND Laparoscopic rectal cancer radical surgery is a complex procedure affected by various factors.However,the existing literature lacks standardized parameters for the pelvic region and soft tissues,which hampers the establishment of consistent conclusions.AIM To comprehensively assess 16 pelvic and 7 soft tissue parameters through computerized tomography(CT)-based three-dimensional(3D)reconstruction,providing a strong theoretical basis to address challenges in laparoscopic rectal cancer radical surgery.METHODS We analyzed data from 218 patients who underwent radical laparoscopic surgery for rectal cancer,and utilized CT data for 3D pelvic reconstruction.Specific anatomical points were carefully marked and measured using advanced 3D modeling software.To analyze the pelvic and soft tissue parameters,we emp-loyed statistical methods including paired sample t-tests,Wilcoxon rank-sum tests,and correlation analysis.RESULTS The investigation highlighted significant sex disparities in 14 pelvic bone parameters and 3 soft tissue parameters.Males demonstrated larger measurements in pelvic depth and overall curvature,smaller measurements in pelvic width,a larger mesorectal fat area,and a larger anterior-posterior abdominal diameter.By contrast,females exhibited wider pelvises,shallower depth,smaller overall curvature,and an increased amount of subcutaneous fat tissue.However,there were no significant sex differences observed in certain parameters such as sacral curvature height,superior pubococcygeal diameter,rectal area,visceral fat area,waist circumference,and transverse abdominal diameter.CONCLUSION The reconstruction of 3D CT data enabled accurate pelvic measurements,revealing significant sex differences in both pelvic and soft tissue parameters.This study design offer potential in predicting surgical difficulties and creating personalized surgical plans for male rectal cancer patients with a potentially“difficult pelvis”,ultimately improving surgical outcomes.Further research and utilization of these parameters

关键词： Computerized tomography Rectal cancer Three-dimensional reconstruction Pelvimetry Sex differences

BMP9 induces osteogenic differentiation through up-regulating LGR4 via the mTORC1/ Stat3 pathway in mesenchymal stem cells

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Genes & Diseases 2024年第3期11卷 468-483页

作者： Jie Zhang Jinhai Jiang Hang Liu Shiyu Wang Kaixin Ke Siyuan Liu Yue Jiang Lu Liu Xiang Gao Baicheng He Yuxi Su department of Pharmacology School of PharmacyChongqing Medical UniversityChongqing 400016China Key Laboratory of Biochemistry and Molecular Pharmacology of Chongqing Chongqing Medical UniversityChongqing 400016China department of Orthopedics Second Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China orthopedics department Children's Hospital of Chongqing Medical UniversityChongqing 400014China China International Science and Technology Cooperation base of Child development and Critical Disorders Jiangxi Hospital Affiliated Children's Hospital of Chongqing Medical UniversityJiangxi 330000China National Clinical Research Center for Child Health and Disorders China

Bone defects and non-union are prevalent in clinical orthopedy,and the outcomes of current treatments are often suboptimal.Bone tissue engineering offers a promising approach to treating these conditions effectively.Bone morphogenetic protein 9(BMP9)can commit mesenchymal stem cells to osteogenic lineage,and a knowledge of the underlying mechanisms may help advance the field of bone tissue engineering.Leucine-rich repeats con-taining G protein-coupled receptor 4(LGR4),a member of G protein-coupled receptors,is essential for modulating bone development.This study is aimed at investigating the impact of LGR4 on BMP9-induced osteogenesis in mesenchymal stem cells as well as the underlying mechanisms.Bone marrow stromal cells from BMp9-knockout mice exhibited diminished LGR4 expression,and exogenous LGR4 clearly restored the impaired osteogenic potency of the bone marrow stromal cells.Furthermore,LGR4 expression was increased by BMP9 in C3H10T1/2 cells.LGR4 augmented the benefits of BMP9-induced osteogenic markers and bone formation,whereas LGR4 inhibition restricted these effects.Meanwhile,the BMP9-induced li-pogenic markers were increased by LGR4 inhibition.The protein levels of Raptor and p-Stat3 were elevated by BMP9.Raptor knockdown or p-Stat3 suppression attenuated the osteoblastic markers and LGR4 expression brought on by BMP9.LGR4 significantly reversed the blocking ef-fect of Raptor knockdown or p-Stat3 suppression on the BMP9-induced osteoblastic markers.Raptor interacts with p-Stat3,and p-Stat3 activates the LGR4 promoter activity.In conclusion,LGR4 boosts BMP9 osteoblastic potency in mesenchymal stem cells,and BMP9 may up-regulate LGR4 via the mTORC1/Stat3 signal activation.

关键词： BMP9 LGR4 mTORC1 Osteogenic differentiation Stat3