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Artemisia argyi extract subfraction exerts an antifungal effect against dermatophytes by disrupting mitochondrial morphology and function

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Chinese Journal of Natural Medicines 2024年第1期22卷 47-61页

作者： CHEN Le ZHU Yunyun GUO Chaowei GUO Yujie ZHAO Lu MIAO Yuhuan DU Hongzhi LIU Dahui College of Pharmacy Hubei University of Chinese MedicineWuhan 430065China National Resource Center for Chinese Materia Medica China Academy of Chinese Medical SciencesBeijing 100700China College of Pharmacy Nanjing University of Chinese MedicineNanjing 210023China

Artemisia argyi(***),a plant with a longstanding history as a raw material for traditional medicine and functional diets in Asia,has been used traditionally to bathe and soak feet for its disinfectant and itch-relieving *** its widespread use,scientific evidence validating the antifungal efficacy of *** water extract(AAWE)against dermatophytes,particularly Trichophyton rubrum,Trichophyton mentagrophytes,and Microsporum gypseum,remains *** study aimed to substantiate the scientific basis of the folkloric use of *** by evaluating the antifungal effects and the underlying molecular mechanisms of its active subfraction against *** results indicated that AAWE exhibited excellent antifungal effects against the three aforementioned dermatophyte *** subfraction AAWE6,isolated using D101 macroporous resin,emerged as the most potent *** minimum inhibitory concentrations(MICs)of AAWE6 against ***,***,and *** were 312.5,312.5,and 625μg·mL−1,*** electron microscopy(TEM)results and assays of enzymes linked to cell wall integrity and cell membrane function indicated that AAWE6 could penetrate the external protective barrier of ***,creating breaches(“small holes”),and disrupt the internal mitochondrial structure(“granary”).Furthermore,transcriptome data,quantitative real-time PCR(RT-qPCR),and biochemical assays corroborated the severe disruption of mitochondrial function,evidenced by inhibited tricarboxylic acid(TCA)cycle and energy ***,chemical characterization and molecular docking analyses identified flavonoids,primarily eupatilin(131.16±4.52 mg·g^(−1))and jaceosidin(4.17±0.18 mg·g^(−1)),as the active components of *** conclusion,the subfraction AAWE6 from *** exerts antifungal effects against dermatophytes by disrupting mitochondrial morphology and *** research validates the traditional use of *** and provides scient

关键词： Artemisia argyi Dermatophyte Antifungal activity mitochondrial structure mitochondrial function Transcriptome analysis

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Synergistic activation of AMPK by AdipoR1/2 agonist and inhibitor of EDPs-EBP interaction recover NAFLD through enhancing mitochondrial function in mice

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Acta Pharmaceutica Sinica B 2023年第2期13卷 542-558页

作者： Nazi Song Hongjiao Xu Shuohan Wu Suijia Luo Jingyao Xu Qian Zhao Rui Wang Xianxing Jiang School of Pharmaceutical Sciences Sun Yat-sen UniversityGuangzhou 511400China State Key Laboratory of Bioactive Substance and function of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100050China School of Life Sciences Key Laboratory of Preclinical Study for New Drugs of Gansu ProvinceSchool of Basic Medical Sciences&Research Unit of Peptide ScienceLanzhou UniversityLanzhou 730000China Shenzhen Turier Biotech.Co. Ltd.Shenzhen 518118China

Nonalcoholic fatty liver disease(NAFLD),especially nonalcoholic steatohepatitis(NASH),is a common hepatic manifestation of metabolic ***,there are no effective therapy to treat this devastating *** evidence suggests that the generation of elastin-derived peptides(EDPs)and the inhibition of adiponectin receptors(Adipo R)1/2 plays essential roles in hepatic lipid metabolism and liver *** recently reported that the AdipoR1/2 dual agonist JT003 significantly degraded the extracellular matrix(ECM)and ameliorated liver ***,the degradation of the ECM lead to the generation of EDPs,which could further alter liver homeostasis ***,in this study,we successfully combined AdipoR1/2 agonist JT003 with V14,which acted as an inhibitor of EDPs-EBP interaction to overcome the defect of ECM *** found that combination of JT003 and V14 possessed excellent synergistic benefits on ameliorating NASH and liver fibrosis than either alone since they compensate the shortage of each *** effects are induced by the enhancement of the mitochondrial antioxidant capacity,mitophagy,and mitochondrial biogenesis via AMPK ***,specific suppression of AMPK could block the effects of the combination of JT003 and V14 on reduced oxidative stress,increased mitophagy and mitochondrial *** positive results suggested that this administration of combination of AdipoR1/2 dual agonist and inhibitor of EDPs-EBP interaction can be recommended alternatively for an effective and promising therapeutic strategy for the treatment of NAFLD and NASH related fibrosis.

关键词： NASH Liver fibrosis Combination therapy mitochondrial function Mitophagy mitochondrial biogenesis AMPK EDPs AdipoR1/2 agonist

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Dietary N-carbamylglutamate or L-arginine supplementation improves hepatic energy status and mitochondrial function and inhibits the AMP-activated protein kinase-peroxisome proliferator- activated receptor γ coactivator-1α-transcription factor A pathway in intrauterine-growth-retarded suckling lambs

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Animal Nutrition 2021年第3期7卷 859-867页

作者： Hao Zhang Xiaoyun Liu Shengnan Ren Mabrouk Elsabagh Mengzhi Wang Hongrong Wang Laboratory of Metabolic Manipulation of Herbivorous Animal Nutrition College of Animal Science and TechnologyYangzhou UniversityYangzhou225009China Joint International Research Laboratory of Agriculture and Agri-Product Safety The Ministry of Education of ChinaYangzhou UniversityYangzhou225009China Department of Animal Production and Technologies Faculty of Agricultural Sciences and TechnologiesNigde Omer Halisdemir UniversityCampusNigde51240Turkey Department of Nutrition and Clinical Nutrition Faculty of Veterinary MedicineKafrelsheikh UniversityKafr El-SheikhEgypt

The objective of this study was to investigate the effects of dietary administration of L-arginine(Arg)or N-carbamylglutamate(NCG)on hepatic energy status and mitochondrial functions in suckling Hu lambs with intrauterine growth retardation(IUGR).Forty-eight newborn Hu lambs of 7 d old were allocated into 4 treatment groups of 12 lambs each,in triplicate with 4 lambs per replicate(2 males and 2 females)as follows:CON(lambs of normal birth weight,4.25±0.14 kg),IUGR(3.01±0.12 kg),IUGR+1%Arg(2.99±0.13 kg),or IUGR+0.1%NCG(3.03±0.11 kg).The experiment lasted for 21 d,until d 28 after birth,and all lambs were fed milk replacer as a basal *** with IUGR lambs,NCG or Arg administration increased(Pmitochondrial function and inhibited the AMPK-PGC1α-TFAM pathway in IUGR suckling lambs.

关键词： L-Arginine Liver Intrauterine growth restriction Energy status mitochondrial function N-carbamylglutamate

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Effects of dietary tributyrin on intestinal mucosa development,mitochondrial function and AMPK-mTOR pathway in weaned pigs

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Journal of Animal Science and Biotechnology 2020年第2期11卷 602-610页

作者： Chunchun Wang Shuting Cao Zhuojun Shen Qihua Hong Jie Feng Yan Peng Caihong Hu Key Laboratory of Molecular Animal Nutrition Ministry of EducationAnimal Science CollegeZhejiang UniversityYu Hang Tang Rd No.866Hangzhou 310058People’s Republic of China Shanghai Menon Animal Nutrition Technology Co.Ltd. Shanghai 201807China

Background:The objective of this experiment was to investigate the influence of dietary tributyrin on intestinal mucosa development,oxidative stress,mitochondrial function and AMPK-mTOR signaling ***:Seventy-two pigs were divided into two treatments and received either a basal diet or the same diet supplemented with 750 mg/kg *** treatment has six replicates of six *** 14 days,6 pigs from each treatment were selected and the jejunal samples were ***:Results showed that supplemental tributyrin increased(Pmitochondrial function,as demonstrated by decreased(Pmitochondrial membrane ***,tributyrin increased(Pmitochondrial DNA content and the mRNA abundance of genes related to mitochondrial functions,including peroxisomal proliferator-activated receptor-γcoactivator-1α,mitochondrial transcription factor A,nuclear respiratory factor-1 in the *** with tributyrin elevated(Pmitochondrial function and modulates the AMPK-mTOR signal pathway of weaned pigs.

关键词： AMPK-mTOR signaling pathway Intestinal mucosa development mitochondrial function Tributyrin Weaned pigs

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REAL-TIME MONITORING OF mitochondrial function AND CEREBRAL BLOOD FLOW FOLLOWING FOCAL ISCHEMIA IN RATS

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Journal of Innovative Optical Health Sciences 2008年第1期1卷 63-69页

作者： AMIR LIVNAT MICHAEL TOLMASOV EFRAT BARBIRO-MICHAELY AVRAHAM MAYEVSKY The Mina&Everard Goodman Faculty of Life-Sciences and The Gonda Multidisciplinary Brain Research Center Bar-Ilan University Ramat-Gan 52900Israel

Focal ischemia due to reduction of cerebral blood flow(CBF),creates 2 zones of damage:the core area,which suffers severe damage,and penumbra area,which surrounds the core and suffers intermediate levels of ***:A novel method is introduced,which evaluates mitochondrial function in the core and in the penumbra,during focal cerebral ***:Wistar rats underwent focal cerebral ischemia by middle cerebral artery occlusion(MCAO)for 60 minutes,followed by 60 minutes of *** function was assessed by a unique Multi-Site—Multi-Parametric(MSMP)monitoring system,which measures mitochondrial NADH using fluorometric technique,and CBF using Laser Doppler Flowmetry(LDF).Results:At the onset of occlusion,CBF dropped and NADH increased significantly only in the right *** levels were significantly lower and NADH significantly higher in the core than in the *** reperfusion,CBF and NADH recovered correspondingly to the intensity of ***:Application of the MSMP system can add significant information for the understanding of the cerebral metabolic state under ischemic conditions,with an emphasis on mitochondrial function.

关键词： mitochondrial function cerebral blood flow focal ischemia

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Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation:The crosstalk between AMPK activation and mitochondrial function

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Animal Nutrition 2022年第3期10卷 137-147页

作者： Liuqin He Xihong Zhou Ziping Wu Yanzhong Feng Di Liu Tiejun Li Yulong Yin Hunan Provincial Key Laboratory of Animal Intestinal function and Regulation Laboratory of Animal Nutrition and Human HealthCollege of Life SciencesHunan Normal UniversityChangsha410081China Key Laboratory of Agro-ecological Processes in Subtropical Region Institute of Subtropical AgricultureChinese Academy of SciencesHunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic ProcessChangsha410125China Agricultural and Food Economics Queen's University BelfastNorthern IrelandBT95PXUnited Kingdom Heilongjiang Academy of Academy of Agricultural Sciences Harbin150086China

The study was conducted to investigate the regulatory mechanism of glutamine(Gln)on intestinal inflammation in an Escherichia coli lipopolysaccharide(*** LPS)-induced in vivo and in vitro ***(n=8)weaned at 21 d of age were fed a basal diet(control and LPS groups)or 1%Gln diet(Gln t LPS group)ad libitum for 4 *** d 22,24,26 and 28,piglets in the LPS and Gln t LPS groups were intraperitoneally injected with *** *** porcine epithelial cells(IPEC-J2)(n=6)induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 50-monophosphate-activated protein kinase(AMPK)*** current results showed that compared with the LPS treatment,the Gln t LPS treatment had better growth performance and greater villus height(Pmitochondrial respiratory metabolism and increase(Pmitochondrial membrane *** activity of AMPK was elevated by 70%to 300%in Gln-treated IPEC-J2 cells under LPS challenge or normal *** results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.

关键词： Glutamine Weaned piglet Intestinal inflammation AMPK mitochondrial function

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Hypoglycemic activity of puerarin through modulation of oxidative stress and mitochondrial function via AMPK

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Chinese Journal of Natural Medicines 2020年第11期18卷 818-826页

作者： HOU Bi-Yu ZHAO Yue Rong MA Peng XU Chun-Yang HE Ping YANG Xiu-Ying ZHANG Li QIANG Gui-Fen DU Guan-Hua State Key Laboratory of Bioactive Substance and function of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College and Beijing Ke|Laboralory of Drug Target and Screening ResearchBeijing 100050China Beiing Obstetrics and Gynecology Hospital Capital Medical UniversityBeijing 100026China

Hyperglycemia is the dominant phenotype of diabetes and the main contributor of diabetic complications. Puerarin is widely used in cardiovascular diseases and diabetic vascular complications. However, little is known about its direct effects on diabetes. The aim of our study is to investigate its antidiabetic effect in vivo and in vitro, and explore the underlying mechanism. We used type I diabetic mice induced by streptozotocin to observe the effects of puerarin on glucose metabolism. In addition, oxidative stress and hepatic mitochondrial respiratory activity were evaluated in type I diabetic mice. In vitro, glucose consumption in Hep G2 cells was assayed along with the q PCR detection of glucogenesis genes expression. Moreover, ATP production was examined and phosphorylation of AMPK was determined using Western blot. Finally, the molecular docking was performed to predict the potential interaction of puerarin with AMPK utilizing program Lib Dock of Discovery Studio 2018 software. The results showed that puerarin improved Hep G2 glucose consumption and upregulated the glucogenesis related genes expression. Also, puerarin lowered fasting and fed blood glucose with improvement of glucose tolerance in type I diabetic mice. Further mechanism investigation showed that puerarin suppressed oxidative stress and improved hepatic mitochondrial respiratory function with enhancing ATP production and activating phosphorylation of AMPK. Docking study showed that puerarin interacted with AMPK activate site and enhancing phosphorylation. Taken together, these findings indicated that puerarin exhibited the hypoglycemic effect through attenuating oxidative stress and improving mitochondrial function via AMPK regulation, which may serve as a potential therapeutic option for diabetes treatment.

关键词： Puerarin Diabetes Hypoglycemic Oxidative stress mitochondrial function

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Abnormal mitochondrial function impairs calcium influx in diabetic mouse pancreatic beta cells

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Chinese Medical Journal 2012年第3期125卷 502-510页

作者： Li Fei Porterfield, D. Marshall Zheng Xi-yan Wang Wen-jun Xu Yue Zhang Zong-ming Tsinghua Univ Dept Gen Surg Digest Med Ctr Med SchAffiliated Hosp 1 Beijing 100016 Peoples R China Purdue Univ Birck Bindley Biosci Ctr Dept Agr & Biol Engn Dept Hort & Landscape ArchitectureWeldon Sch Bio W Lafayette IN 47906 USA Beijing Sci & Technol Co Ltd Beijing 100080 Peoples R China

Background Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 *** studies found impaired mitochondrial function and impaired Ca2＋ influx in beta cells in diabetic patients and animal models,suggesting a role for these processes in proper insulin *** aim of this study was to investigate the detailed relationship of mitochondrial function,Ca2＋ influx,and defective insulin *** We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J *** types of Ca2＋ channel activities,L-type and store-operated Ca2＋（SOC）,were evaluated using whole-cell patch-clamp *** glucose induced Ca2＋ influx was measured by a non-invasive micro-test technique （NMT）.Results Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae,and mitochondrial function decreased compared with C57BL/6J ***2＋ channel activity was increased and glucose induced Ca2＋ influx was impaired,but could be recovered by *** Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca2＋ influx,but not via Ca2＋ channel activity.

关键词： type 2 diabetes pancreatic beta cell insulin secretion Ca2+ influx mitochondrial function

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Value of dynamic 31p magnetic resonance spectroscopy technique in in vivo assessment of the skeletal muscle mitochondrial function in type 2 diabetes

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Chinese Medical Journal 2012年第2期125卷 281-286页

作者： WU Fei-yun TU Hui-juan QIN Bin CHEN Ting XU Hua-feng QI Jing WANG De-hang Department of Radiology the First Affiliated Hospital of Nanjing Medical University Nanjing Jiangsu 210029 China

Background Phosphorous magnetic resonance spectroscopy （31p-MRS） has been successfully applied to study intracellular membrane compounds and high-energy phosphate *** study aimed to evaluate the capability of dynamic 31p-MRS for assessing energy metabolism and mitochondrial function in skeletal muscle from type 2 diabetic *** Dynamic 31p-MRS was performed on 22 patients with type 2 diabetes and 26 healthy *** were acquired from quadriceps muscle while subjects were in a state of rest,at exercise and during *** peak areas of inorganic phosphate （Pi）,phosphocreatine （PCr）,and adenosine triphosphate （ATP） were *** concentration of adenosine diphosphate （ADP） and the intracellular pH value were calculated from the biochemistry reaction *** time constant and recovery rates of Pi,PCr,and ADP were analyzed using exponential curve *** As compared to healthy controls,type 2 diabetes patients had significantly lower skeletal muscle concentrations of Pi,PCr and β-ATP,and higher levels of ADP and Pi/*** exercise,diabetics experienced a significant Pi peak increase and PCr peak decrease,and once the exercise was completed both Pi and PCr peaks returned to resting ***,the mean recovery rates of Pi and PCr in diabetes patients were （10.74±1.26） mmol/s and （4.74±2.36） mmol/s,respectively,which was significantly higher than in *** Non-invasive quantitative 31P-MRS is able to detect energy metabolism inefficiency and mitochondrial function impairment in skeletal muscle of type 2 diabetics.

关键词： type 2 diabetes phosphorus magnetic resonance spectroscopy skeletal muscle mitochondrial function

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Regulation of mitochondrial function and endoplasmic reticulum stress by nitric oxide in pluripotent stem cells

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World Journal of Stem Cells 2017年第2期9卷 26-36页

作者： Estefania Caballano-Infantes José Terron-Bautista Amparo Beltrán-Povea Gladys M Cahuana Bernat Soria Hajji Nabil Francisco J Bedoya Juan R Tejedo Andalusian Center for Molecular Biology and Regenerative Medicine-University Pablo de Olavide 41092 SevilleSpain Biomedical Research Network on Diabetes and Related Metabolic Diseases(CIBERDEM) Instituto de Salud CarlosⅢ28029 MadridSpain Andalusian Center for Molecular Biology and Regenerative Medicine(CABIMER) 41092 SevilleSpain Andalusian Center for Molecular Biology and Regenerative Medicine Fundación Progreso y Salud41092 SevilleSpain Centre for Pharmacology and Therapeutics Division of Experimental MedicineImperial College LondonHammersmith Hospital CampusLondon W12 0NNUnited Kingdom

mitochondrial dysfunction and endoplasmic reticulum stress(ERS) are global processes that are interrelated and regulated by several stress factors. Nitric oxide(NO) is a multifunctional biomolecule with many varieties of physiological and pathological functions, such as the regulation of cytochrome c inhibition and activation of the immune response, ERS and DNA damage; these actions are dose-dependent. It has been reported that in embryonic stem cells, NO has a dual role, controlling differentiation, survival and pluripotency, but the molecular mechanisms by which it modulates these functions are not yet known. Low levels of NO maintain pluripotency and induce mitochondrial biogenesis. It is well established that NO disrupts the mitochondrial respiratory chain and causes changes in mitochondrial Ca^(2+) flux that induce ERS. Thus, at high concentrations, NO becomes a potential differentiation agent due to the relationship between ERS and the unfolded protein response in many differentiated cell lines. Nevertheless, many studies have demonstratedthe need for physiological levels of NO for a proper ERS response. In this review, we stress the importance of the relationships between NO levels, ERS and mitochondrial dysfunction that control stem cell fate as a new approach to possible cell therapy strategies.

关键词： Endoplasmic reticulum stress mitochondrial function Nitric oxide Pluripotency Cell differentiation mitochondrial biogenesis

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