ABSTRACT
Many recent studies have shown that the gut microbiome plays important roles in human physiology and pathology. Also, microbiome-based therapies have been used to improve health status and treat diseases. In addition, aging and neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, have become topics of intense interest in biomedical research. Several researchers have explored the links between these topics to study the potential pathogenic or therapeutic effects of intestinal microbiota in disease. But the exact relationship between neurodegenerative diseases and gut microbiota remains unclear. As technology advances, new techniques for studying the microbiome will be developed and refined, and the relationship between diseases and gut microbiota will be revealed. This article summarizes the known interactions between the gut microbiome and neurodegenerative diseases, highlighting assay techniques for the gut microbiome, and we also discuss the potential therapeutic role of microbiome-based therapies in diseases.
ABSTRACT
Many recent studies have shown that the gut microbiome plays important roles in human physiology and pathology. Also, microbiome-based therapies have been used to improve health status and treat diseases. In addition, aging and neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, have become topics of intense interest in biomedical research. Several researchers have explored the links between these topics to study the potential pathogenic or therapeutic effects of intestinal microbiota in disease. But the exact relationship between neurodegenerative diseases and gut microbiota remains unclear. As technology advances, new techniques for studying the microbiome will be developed and refined, and the relationship between diseases and gut microbiota will be revealed. This article summarizes the known interactions between the gut microbiome and neurodegenerative diseases, highlighting assay techniques for the gut microbiome, and we also discuss the potential therapeutic role of microbiome-based therapies in diseases.
Subject(s)
Humans , Alzheimer Disease/therapy , Gastrointestinal Microbiome , Microbiota , Neurodegenerative Diseases/therapy , Parkinson Disease/therapyABSTRACT
Objective@#To understand the awareness and influencing factors of medical healthcare APP among female college students in Weifang, and to provide references for healthy lifestyle and health literacy improvement.@*Methods@#A total of 891 female college students were selected by stratified random sampling method, and were investigated regrading awareness on medical and health care APP and associated factors. Data were statistically analyzed by composition ratio, CHI-square test and binary Logistic regression.@*Results@#There were 54.6% of the female college students who reported not aware of medical healthcare APP. The overall awareness rates of medical and health care APP for freshmen,sophomores, juniors, seniurs and above were 39.75%,45.59%,55.78% and 52.56%, respectively, and the difference was statistically significant(χ2=16.43，P<0.05). Logistic regression analysis showed that medical costs, medical healthcare information attention, medical health care information recognition, consulting the treatment scheme were positively associated with awareness of health care APP(OR=1.40,1.51,1.27,1.33,P<0.05).@*Conclusion@#The awareness rate of medical health care APP of female college students in Weifang is relatively low,and the difference between different groups is obvious. It is necessary to improve the scientific knowledge rate of the female college students to the APP, so as to influence the life style of the female college students.
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Objective To investigate the effect of prostaglandin E2 receptor 1 (EP1) on Adriamycin (ADR)-induced glomerular podocytes injury and its possible mechanism.Methods (1) In vivo experiments:6-8 weeks old male Balb/c mice were randomly divided into four groups:Control group;ADR group;EP1 agonist 17-phenyl PGE2+ADR group;EP1 antagonist SC-19220+ADR group.The mouse model of nephrotic syndrome was induced by injection of ADR (10 mg/kg) into tail vein,and then EP1 agonist (1 μg/g) and antagonist (25 μg/g) were administered respectively.Six weeks later,all mice were sacrificed and urine,blood and kidney tissues were collected.Detecting urine protein,blood chemistry,changes of renal pathology and podocyte-related proteins,electron microscopy changes of podocytes.(2) In vitro experiments:Podocytes were cultured in vitro and divided into different groups:Control group;ADR group (0.2 μmol/L);EP1 agonist (0.1,1,10 μmol/L)+ADR (0.2 μmol/L) group;antagonist (0.1,0.5,1 μmol/L)+ ADR (0.2 μmol/L) group.The proliferation of podocytes was measured by CCK-8.Expression of PGE2 in podocytes was detected by ELISA.Indirect immunofluorescence was used to determine the localization of podocyte-related proteins nephrin,podocin and CD2AP.Expression of nephrin,podocin,CD2AP,COX2 in podocytes was detected by Western blotting and Real-time quantitative PCR.p38 MAPK or phospho-p38 MAPK was measured by Western blotting as well.Flow cytometry was used to detect cell apoptosis.Results (1) In vivo experiments:Compared with control group,obvious proteinuria,blood biochemical changes and renal pathological changes were observed in ADR group,proteinuria,blood biochemical and renal pathological changes were more serious in mice dealt with agonist,while antagonist could reduce ADR-induced injury (all P ＜ 0.05).Results of immunohistochemistry showed that the expression of podocyterelated proteins nephrin,podocin and CD2AP in ADR group were significantly lower than those in control group,and EP1 agonist could further inhibit expression of these proteins,while antagonist could reverse this inhibitory effects (P ＜ 0.05).Electron microscopic results showed that mice in ADR group appeared foot enlargement and fusion,and the agonist group further aggravated the injury,while antagonist intervention could inhibit the injury of podocytes.(2) In vitro experiments:Compared with control group,expression of PGE2 and COX2 were increased;mRNA and protein expression of nephrin,podocin,CD2AP were decreased,p38 MAPK activity and podocytes apoptosis were increased in ADR group (P ＜ 0.05);Agonist could aggravate podocytes damage (P ＜ 0.05),while Antagonist could downregulate the expression of PGE2 and COX2,promote the expression of nephrin,podocin and CD2AP,and inhibit the activity of p38 MAPK and podocytes apoptosis (P ＜ 0.05).The addition of p38 MAPK inhibitor(10 μmol/L) could reduce the inhibitory effect of EP1 agonist on the expression of podocyterelated proteins nephrin,podocin and CD2AP (P ＜ 0.05).Conclusions EP1 receptor may activate the p38 MAPK signaling pathway to inhibit podocytes-related proteins nephrin,podocin and CD2AP,as well as mediate the ADR induced podocyte injury.Inhibition of EP1 receptor however have a protective effect.
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OBJECTIVE@#To examine the structural differences in regional gray matter density between a sample of major depressive disorder (MDD) and healthy controls, using the magnetic resonance imaging (MRI) to find the base of pathophysiologic mechanism in depression development.@*METHODS@#A total of 38 MDD patients and 42 healthy subjects enrolled in the MRI scans. Voxel-based morphometry was used to test the difference in gray matter between the 2 groups.@*RESULTS@#The MDD group showed significantly lower gray density than the healthy control group in the right middle frontal gyrus, right superior frontal gyrus, left inferior frontal gyrus and left superior frontal gyrus. However, the healthy control group showed significantly lower gray density than the MDD group in the right precuneus, left anterior central gyrus and right anterior cingutate.@*CONCLUSION@#Structural brain abnormalities in MDD patients may be the pathological bases for MDD development.