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Potassium dehydroandrographolide succinate regulates the MyD88/CDH13 signaling pathway to enhance vascular injuryinduced pathological vascular remodeling

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Chinese Journal of Natural medicines 2024年第1期22卷 62-74页

作者： GUO Qiru LI Jiali WANG Zheng WU Xiao JIN Zhong ZHU Song LI Hongfei ZHANG Delai HU Wangming XU Huan YANG Lan SHI Liangqin WANG Yong college of basic medicine Chengdu University of Traditional Chinese MedicineChengdu 610000China Chengdu University of Traditional Chinese medicine Hospital of Chengdu University of Traditional Chinese MedicineChengdu 610000China

Pathological vascular remodeling is a hallmark of various vascular diseases.Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction,which leads to pathological vascular remodeling.Potassium dehydroandrographolide succinate(PDA),a derivative of andrographolide,has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections.This study investigates the potential of PDA in regulating pathological vascular remodeling.The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice.Experimental approaches,including rat aortic primary smooth muscle cell culture,flow cytometry,bromodeoxyuridine(BrdU)incorporation assay,Boyden chamber cell migration assay,spheroid sprouting assay,and Matrigel-based tube formation assay,were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells(SMCs).Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions.The results revealed that PDA exacerbates vascular injury-induced pathological remodeling,as evidenced by enhanced neointima formation.PDA treatment significantly increased the proliferation and migration of SMCs.Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88(MyD88)expression in SMCs and interacted with T-cadherin(CDH13).This interaction augmented proliferation,migration,and extracellular matrix deposition,culminating in pathological vascular remodeling.Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling,mediated through the MyD88/CDH13 signaling pathway.

关键词： Potassium dehydroandrographolide succinate Smooth muscle cell Myeloid differentiation factor 88 T-cadherin Pathological vascular remodeling

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Structural characterization and prebiotic potential of polysaccharides from Polygonatum sibiricum

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Food Science and Human Wellness 2024年第4期13卷 2208-2220页

作者： Zihan Qi Tiexiang Gao Jingjing Li Shuhan Zhou Zhigang Zhang Mingzhu Yin Haiming Hu Hongtao Liu college of basic Medical Sciences Hubei University of Chinese MedicineWuhan 430065China college of Pharmacy Hubei University of Chinese MedicineWuhan 430065China

Polygonatum sibiricum has been widely used due to its excellent biological activities.We prepared a novel polysaccharide from P.sibiricum(PSP)in this study.According a monosaccharide composition analysis,PSP was mainly composed of fructose and glucose with a molar percentage of 93.81:5.12.The main linkage types were identified asα-D-Glcp-1→and→2-β-D-Fruf-1→.The molecular weight of PSP showed no significant change after simulated salivary and gastrointestinal digestion.However,PSP could be broken down by intestinal bacteria.Our findings revealed that PSP administration increased the abundance of probiotics such as Bifidobacterium.Furthermore,the results showed that gut microbes could utilize PSP to produce short-chain fatty acids including acetic acid,propionic acid,and butyric acid.Also,the PSP fermentation broth displayed an excellent scavenging effect on free radicals,including 2,2-diphenyl-1-picrylhydrazyl radical,superoxide radical,and hydroxyl radical.In summary,this study will help to promote the application of PSP as prebiotics in functional food and the medical industry.

关键词： Dietary polysaccharides Prebiotic Gut microbiota Short-chain fatty acids

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Vanillylacetone attenuates cadmium chloride-induced hippocampal damage and memory loss through upregulation of nuclear factor erythroid 2-related factor 2 gene and protein expression

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Neural Regeneration Research 2024年第12期19卷 2750-2759页

作者： Fahaid H.A.L-Hashem Salah O.Bashir Amal F.Dawood Moutasem S.Aboonq Ismaeel Bin-Jaliah Abdulaiziz M.Al-Garni Mohamed D.Morsy Department of Physiology College of MedicineKing Khalid UniversityAbhaSaudi Arabia Department of basic Medical Sciences College of MedicinePrincess Nourah bint Abdulrahman UniversityP.O.Box 84428Riyadh 11671Saudi Arabia Department of Physiology College of MedicineTaibah UniversityAl-Madinah Al-MunawwarahSaudi Arabia Department of medicine College of MedicineKing Khalid UniversityAbhaSaudi Arabia

Memory loss and dementia are major public health concerns with a substantial economic burden.Oxidative stress has been shown to play a crucial role in the pathophysiology of hippocampal damage-induced memory impairment.To investigate whether the antioxidant and anti-inflammatory compound vanillyla cetone(zingerone) can protect against hippocampal damage and memory loss induced by cadmium chloride(CdCl_(2)) administration in rats,we explo red the potential involvement of the nuclear factor erythroid 2-related factor 2(Nrf2) signaling pathway,which is known to modulate oxidative stress and inflammation.Sixty healt hy male Wistar rats were divided into five groups:vehicle-treated(control),vanillylacetone,CdCl_(2),vanillylacetone+ CdCl_(2),vanillylacetone+ CdCl_(2)+ brusatol(a selective pharmacological N rf2inhibitor) groups.Vanillylacetone effectively attenuated CdCl_(2)-induced damage in the dental gyrus of the hippocampus and improved the memory function assessed by the Morris Water Maze test.Additionally,vanillylacetone markedly decreased the hippocampal tissue levels of inflammatory biomarkers(interleukin-6,tumor necrosis factor-α,intracellular cell adhesive molecules) and apoptosis biomarkers(Bax and cleaved caspase-3).The control and CdCl_(2)-treated groups treated with va nillylacetone showed reduced generation of reactive oxygen species,decreased malondialdehyde levels,and increased superoxide dismutase and glutathione activities,along with significant elevation of nuclear Nrf2 mRNA and protein expression in hippocampal tissue.All the protective effects of vanillylacetone we re substantially blocked by the co-administration of brusatol(a selective N rf2 inhibitor).Va nillylacetone mitigated hippocampal damage and memory loss induced by CdCl_(2),at least in part, by activating the nuclear transcription factor Nrf2.Additionally,vanillylacetone exerted its potent antioxidant and antiinflammatory actions.

关键词： hippocampus neuroprotective Nrf2 gene oxidative stress vanillylacetone

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Yemazhui(Herba Eupatorii Lindleyani)ameliorates lipopolysaccharide-induced acute lung injury via modulation of the toll-like receptor 4/nuclear factor kappa-B/nod-like receptor family pyrin domain-containing 3 protein signaling pathway and intestinal flor

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Journal of Traditional Chinese medicine 2024年第2期44卷 303-314页

作者： REN Li HAI Yang YANG Xue LUO Xianqin Chongqing Key Laboratory of Traditional Chinese medicine for Prevention and Cure of Metabolic Diseases College of Traditional Chinese MedicineChongqing Medical UniversityChongqing 400016China college of basic medicine Chongqing Medical UniversityChongqing 400016China

OBJECTIVE:To investigate the impact of Yemazhui(Herba Eupatorii Lindleyani,HEL)against lipopolysaccharide(LPS)-induced acute lung injury(ALI)and explore its underlying mechanism in vivo.METHODS:The chemical constituents of HEL were analyzed by ultra-high performance liquid chromatographyquadrupole time-of-flight mass spectrometry method.Then,HEL was found to suppress LPS-induced ALI in vivo.Six-week-old male Sprague-Dawley rats were randomly divided into 6 groups:control,LPS,Dexamethasone(Dex),HEL low dose 6 g/kg(HEL-L),HEL medium dose 18 g/kg(HEL-M)and HEL high dose 54 g/kg(HEL-H)groups.The model rats were intratracheally injected with 3 mg/kg LPS to establish an ALI model.Leukocyte counts,lung wet/dry weight ratio,as well as myeloperoxidase(MPO)activity were determined followed by the detection with hematoxylin and eosin staining,enzyme linked immunosorbent assay,quantitative real time polymerase chain reaction,western blotting,immunohistochemistry,and immunofluorescence.Besides,to explore the effect of HEL on ALI-mediated intestinal flora,we performed 16s rRNA sequencing analysis of intestinal contents.RESULTS:HEL attenuated LPS-induced inflammation in lung tissue and intestinal flora disturbance.Mechanism study indicated that HEL suppressed the lung coefficient and wet/dry weight ratio of LPS-induced ALI in rats,inhibited leukocytes exudation and MPO activity,and improved the pathological injury of lung tissue.In addition,HEL reduced the expression of tumor necrosis factoralpha,interleukin-1beta(IL-1β)and interleukin-6(IL-6)in bronchoalveolar lavage fluid and serum,and inhibited nuclear displacement of nuclear factor kappa-B p65(NF-κBp65).And 18 g/kg HEL also reduced the expression levels of toll-like receptor 4(TLR4),myeloid differentiation factor 88,NF-κBp65,phosphorylated inhibitor kappa B alpha(phospho-IκBα),nod-like receptor family pyrin domain-containing 3 protein(NLRP3),IL-1β,and interleukin-18(IL-18)in lung tissue,and regulated intestinal flora disturbance.CONCLUSIONS:In summary,our findings revealed

关键词： Yemazhui(Herba Eupatorii Lindleyani) acute lung injury anti-inflammation toll-like receptor 4 nuclear factor kappa-B nod-like receptor family pyrin domain-containing 3 protein signal transduction gastrointestinal microbiome

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Electroacupuncture Promotes Angiogenesis in Mice with Cerebral Ischemia by Inhibiting miR-7

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Chinese Journal of Integrative medicine 2024年第6期30卷 543-550页

作者： YU Qian SHU Shi JU Xin-yao PENG Wei REN Xue-qi SI Shu-han SONG Shi-zhen XIE Xue-yun FANG Bang-jiang ZHOU Shuang School of Acupuncture-Moxibustion and Tuina Shanghai University of Traditional Chinese MedicineShanghai201203China college of basic medicine Shanghai University of Traditional Chinese MedicineShanghai201203China Department of Emergency Longhua HospitalShanghai University of Traditional Chinese MedicineShanghai200032China

Objective To observe the angiogenesis effect of electroacupuncture(EA)at Shuigou acupoint(GV 26)in the treatment of cerebral ischemia,and explore the value of miRNA-7(miR-7)in it.Methods First,48 mice were randomly divided into sham operation,middle cerebral artery occlusion(MCAO)model,and EA treatment groups.Then 9 mice were divided into carrier control group,miR-7 knockout group and miR-7 overexpression group(n=3 each group).Finally,20 mice were divided into model and carrier control group,model and miR-7 knockout group,EA treatment and carrier control group and EA treatment and miR-7 overexpression group,with 3–6 mice in each group.The MCAO model was established in the MCAO and EA groups.Neurological deficit score and 2,3,5-triphenyltetrazolium chloride(TTC)staining were used to evaluate the severity of cerebral ischemia.Hematoxylin-eosin staining was used to describe basic pathological changes.Immunohistochemistry was used to quantify cerebral microvessel density.Real-time PCR and Western blot were used to detect the expression of miR-7 and its downstream target genes Krüppel-like factor 4/vascular endothelial growth factor(KLF4/VEGF)and angiopoietin-2(ANG-2)in the ischemic cerebral cortex.Results After EA,neurological deficit scores and infarction volumes decreased,and the density of cerebral microvessels increased.In the MCAO group,miR-7 expression was higher than that in the sham group(P<0.01).After EA at GV 26,miR-7 expression decreased(P<0.01)and the expression of downstream target genes KLF4/VEGF and ANG-2 increased as compared with the MCAO group(P<0.01).After EA combined with overexpression of miR-7,the expression of downstream target genes KLF4/VEGF and ANG-2 decreased compared to the control EA group(P<0.01).After miR-7 knockdown,the expression of KLF4/VEGF and ANG-2 increased(P<0.05 or P<0.01).Conclusions EA could promote angiogenesis in MCAO mice likely by inhibiting the expression of miR-7 and relieving inhibition of downstream target genes KLF4/VEGF and ANG-2.

关键词： electroacupuncture cerebral ischemia miRNA-7 angiogenesis Shuigou(GV 26) acupuncture points

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Herb pair of Huangqi-Danggui exerts anti-tumor immunity to breast cancer by upregulating PIK3R1

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Animal Models and Experimental medicine 2024年第3期7卷 234-258页

作者： Hai-Xin Liu Li Lian Li-Li Hou Cai-Xia Liu Jin-Hong Ren Yuan-Biao Qiao Shi-Yuan Wen Qing-Shan Li college of Traditional Chinese medicine and Food Engineering Shanxi University of Chinese MedicineTaiyuanChina Shanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation College of Traditional Chinese Medicine and Food EngineeringShanxi University of Chinese MedicineTaiyuanChina college of basic Medical Sciences Shanxi Medical UniversityTaiyuanChina

Background:According to traditional Chinese medicine(TCM),drugs supplementing the vital energy,Qi,can eliminate tumors by restoring host immunity.The objective of this study is to investigate the underlying immune mechanisms of anti-tumor activity associated with Qi-supplementing herbs,specifically the paired use of Huangqi and Danggui.Methods:Analysis of compatibility regularity was conducted to screen the combination of Qi-supplementing TCMs.Using the MTT assay and a transplanted tumor mice model,the anti-tumor effects of combination TCMs were investigated in vitro and in vivo.High content analysis and flow cytometry were then used to evaluate cellular immunity,followed by network pharmacology and molecular docking to dissect the significant active compounds and potential mechanisms.Finally,the anti-tumor activity and the mechanism of the active ingredients were verified by molecular experiments.Results:There is an optimal combination of Huangqi and Danggui that,administered as an aqueous extract,can activate immunity to suppress tumor and is more effective than each drug on its own in vitro and in vivo.Based on network pharmacology analysis,PIK3R1 is the core target for the anti-tumor immunity activity of combined Huangqi and Danggui.Molecular docking analysis shows 6 components of the combined Danggui and Huangqi extract(quercetin,jaranol,isorhamnetin,kaempferol,calycosin,and suchilactone)that bind to PIK3R1.Jaranol is the most important component against breast cancer.The suchilactone/jaranol combination and,especially,the suchilactone/kaempferol combination are key for immunity enhancement and the anti-tumor effects of the extract.Conclusions:The combination of Huangqi and Danggui can activate immunity to suppress breast cancer and is more effective than the individual drugs alone.

关键词： anti-tumor Danggui Huangqi immunity

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Engineering the spectra of photon triplets generated from micro/nanofiber

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Chinese Physics B 2024年第3期33卷 408-414页

作者：瞿川郭东琴李笑笑刘振旗赵义张胜海卫正统 The college of basic Department Information Engineering UniversityZhengzhou 450000China

Quantum light sources are the core resources for photonics-based quantum information processing.We investigate the spectral engineering of photon triplets generated by third-order spontaneous parametric down-conversion in micro/nanofiber.The phase mismatching at one-third pump frequency gives rise to non-degenerate photon triplets,the joint spectral intensity of which has an elliptical locus with a fixed eccentricity of√6/3.Therefore,we propose a frequency-division scheme to separate non-degenerate photon triplets into three channels with high heralding efficiency for the first time.Choosing an appropriate pump wavelength can compensate for the fabrication errors of micro/nanofiber and also generate narrowband,non-degenerate photon triplet sources with a high signal-to-noise ratio.Furthermore,the long-period micro/nanofiber grating introduces a new controllable degree of freedom to tailor phase matching,resulting from the periodic oscillation of dispersion.In this scheme,the wavelength of photon triplets can be flexibly tuned using quasi-phase matching.We study the generation of photon triplets from this novel perspective of spectrum engineering,and we believe that this work will accelerate the practical implementation of photon triplets in quantum information processing.

关键词： photon triplets micro/nanofiber spectrum engineering

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Development of a new cerebral ischemia reperfusion model of Mongolian gerbils and standardized evaluation system

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Animal Models and Experimental medicine 2024年第1期7卷 48-55页

作者： Ying Wu Caijiao Hu Zhihui Li Feiyang Li Jianyi Lv Meng Guo Xin Liu Changlong Li Xueyun Huo Zhenwen Chen Lifeng Yang Xiaoyan Du School of basic Medical Sciences Capital Medical UniversityBeijingChina Laboratory for Clinical medicine Capital Medical UniversityBeijingChina college of Veterinary medicine China Agricultural UniversityBeijingChina

Background:The Mongolian gerbil is an excellent laboratory animal for preparing the cerebral ischemia model due to its inherent deficiency in the circle of Willis.However,the low incidence and unpredictability of symptoms are caused by numerous complex variant types of the circle.Additionally,the lack of an evaluation system for the cer-ebral ischemia/reperfusion(I/R)model of gerbils has shackled the application of this model.Methods:We created a symptom-oriented principle and detailed neurobehavioral scoring criteria.At different time points of reperfusion,we analyzed the alteration in locomotion by rotarod test and grip force score,infarct volume by triphenyltetrazo-lium chloride(TTC)staining,neuron loss using Nissl staining,and histological charac-teristics using hematoxylin-eosin(H&E)straining.Results:With a successful model rate of 56%,32 of the 57 gerbils operated by our method harbored typical features of cerebral I/R injury,and the mortality rate in the male gerbils was significantly higher than that in the female gerbils.The suc-cessfully prepared I/R gerbils demonstrated a significant reduction in motility and grip strength at 1 day after reperfusion;formed obvious infarction;exhibited typi-cal pathological features,such as tissue edema,neuronal atrophy and death,and vacuolated structures;and were partially recovered with the extension of reperfu-sion time.Conclusion:This study developed a new method for the unilateral common carotid artery ligation I/R model of gerbil and established a standardized evaluation system for this model,which could provide a new cerebral I/R model of gerbils with more practical applications.

关键词： ischemia/reperfusion Mongolian gerbil standardized model system unilateral carotid occlusion

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Icariin attenuates vascular endothelial dysfunction by inhibiting inflammation through GPER/Sirt1/HMGB1 signaling pathway in type 1 diabetic rats

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Chinese Journal of Natural medicines 2024年第4期22卷 293-306页

作者： YAO Wenhui TAO Rongpin WANG Kai DING Xuansheng School of basic medicine and Clinical Pharmacy China Pharmaceutical UniversityNanjing211198China

Icariin, a flavonoid glycoside, is extracted from Epimedium. This study aimed to investigate the vascular protective effects of icariin in type 1 diabetic rats by inhibiting high-mobility group box 1 (HMGB1)-related inflammation and exploring its potential mechanisms. The impact of icariin on vascular dysfunction was assessed in streptozotocin (STZ)-induced diabetic rats through vascular reactivity studies. Western blotting and immunofluorescence assays were performed to measure the expressions of target proteins. The release of HMGB1 and pro-inflammation cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The results revealed that icariin administration enhanced acetylcholine-induced vasodilation in the aortas of diabetic rats. It also notably reduced the release of pro-inflammatory cytokines, including interleukin-8 (IL-8), IL-6, IL-1β, and tumor necrosis factor-alpha (TNF-α) in diabetic rats and high glucose (HG)-induced human umbilical vein endothelial cells (HUVECs). The results also unveiled that the pro-inflammatory cytokines in the culture medium of HUVECs could be increased by rHMGB1. The increased release of HMGB1 and upregulated expressions of HMGB1-related inflammatory factors, including advanced glycation end products (RAGE), Toll-like receptor 4 (TLR4), and phosphorylated p65 (p-p65) in diabetic rats and HG-induced HUVECs, were remarkably suppressed by icariin. Notably, HMGB1 translocation from the nucleus to the cytoplasm in HUVECs under HG was inhibited by icariin. Meanwhile, icariin could activate G protein-coupled estrogen receptor (GPER) and sirt1. To explore the role of GPER and Sirt1 in the inhibitory effect of icariin on HMGB1 release and HMGB-induced inflammation, GPER inhibitor and Sirt1 inhibitor were used in this study. These inhibitors diminished the effects of icariin on HMGB1 release and HMGB1-induced inflammation. Specifically, the GPER inhibitor also negated the activation of Sirt1 by icariin. These findings suggest that icariin activates GPER and increases the exp

关键词： Icariin Diabetes Inflammation Vascular endothelial dysfunction GPER HMGB1

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Targeting carnitine palmitoyl transferase 1A(CPT1A)induces ferroptosis and synergizes with immunotherapy in lung cancer

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Signal Transduction and Targeted Therapy 2024年第4期9卷 1675-1689页

作者： Lei Ma Chong Chen Chunxing Zhao Tong Li Lingyu Ma Jiayu Jiang Zhaojun Duan Qin Si Tsung-Hsien Chuang Rong Xiang Yunping Luo Department of Immunology Institute of Basic Medical SciencesChinese Academy of Medical SciencesSchool of Basic MedicinePeking Union Medical CollegeBeijing 100005China Collaborative Innovation Center for Biotherapy Institute of Basic Medical SciencesChinese Academy of Medical SciencesSchool of Basic MedicinePeking Union Medical CollegeBeijing 100005China Department of Lung Cancer Surgery Tianjin Medical University General HospitalTianjin 300052China Immunology Research Center National Health Research InstitutesZhunanMiaoliTaiwanROC Department of Immunology Nankai UniversityTianjin 300071China

Despite the successful application of immune checkpoint therapy,no response or recurrence is typical in lung cancer.Cancer stem cells(CSCs)have been identified as a crucial player in immunotherapy-related resistance.Ferroptosis,a form of cell death driven by iron-dependent lipid peroxidation,is highly regulated by cellular metabolism remolding and has been shown to have synergistic effects when combined with immunotherapy.Metabolic adaption of CsCs drives tumor resistance,yet the mechanisms of their ferroptosis defense in tumor immune evasion remain elusive.Here,through metabolomics,transcriptomics,a lung epithelialspecific Cptla-knockout mouse model,and clinical analysis,we demonstrate that CPT1A,a key rate-limiting enzyme of fatty acid oxidation,acts with L-carnitine,derived from tumor-associated macrophages to drive ferroptosis-resistance and CD8^(+)T cells inactivation in lung cancer.Mechanistically,CPT1A restrains ubiquitination and degradation of c-Myc,while c-Myc transcriptionally activates CPT1A expression.The CPT1A/c-Myc positive feedback loop further enhances the cellular antioxidant capacity by activating the NRF2/GPX4 system and reduces the amount of phospholipid polyunsaturated fatty acids through ACSL4 downregulating,thereby suppressing ferroptosis in CSCs.Significantly,targeting CPT1A enhances immune checkpoint blockadeinduced anti-tumor immunity and tumoral ferroptosis in tumor-bearing mice.The results illustrate the potential of a mechanismguided therapeutic strategy by targeting a metabolic vulnerability in the ferroptosis of CsCs to improve the efficacy of lung cancer immunotherapy.

关键词： immunotherapy metabolism peroxidation

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