Effect of Bu-Zhong-Yi-Qi-Tang on deficiency of N-glycan/nitric oxide and islet damage induced by streptozotocin indiabetic rats

Liu, Xiaoqiu; Wu, Ling; Guo, Xuejun

doi:10.3748/wjg.15.1730

Cited by 13 publications

(10 citation statements)

References 21 publications

(19 reference statements)

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“…[39][40][41][42] N-glycan deficiency in glycoproteins has been linked to islet damage and T2D. [43][44][45] TGF-b signaling has been implicated to be important for pancreatic islet development. 46,47 Islet-toislet or b-to-b cell communication has shown to be the basis for insulin secretion.…”

mentioning

confidence: 99%

Integrating Pathway Analysis and Genetics of Gene Expression for Genome-wide Association Studies

Zhong

Yang

Kaplan

et al. 2010

The American Journal of Human Genetics

222

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Genome-wide association studies (GWAS) have achieved great success identifying common genetic variants associated with common human diseases. However, to date, the massive amounts of data generated from GWAS have not been maximally leveraged and integrated with other types of data to identify associations beyond those associations that meet the stringent genome-wide significance threshold. Here, we present a novel approach that leverages information from genetics of gene expression studies to identify biological pathways enriched for expression-associated genetic loci associated with disease in publicly available GWAS results. Specifically, we first identify SNPs in population-based human cohorts that associate with the expression of genes (eSNPs) in the metabolically active tissues liver, subcutaneous adipose, and omental adipose. We then use this functionally annotated set of SNPs to investigate pathways enriched for eSNPs associated with disease in publicly available GWAS data. As an example, we tested 110 pathways from the Kyoto Encylopedia of Genes and Genomes (KEGG) database and identified 16 pathways enriched for genes corresponding to eSNPs that show evidence of association with type 2 diabetes (T2D) in the Wellcome Trust Case Control Consortium (WTCCC) T2D GWAS. We then replicated these findings in the Diabetes Genetics Replication and Meta-analysis (DIAGRAM) study. Many of the pathways identified have been proposed as important candidate pathways for T2D, including the calcium signaling pathway, the PPAR signaling pathway, and TGF-beta signaling. Importantly, we identified other pathways not previously associated with T2D, including the tight junction, complement and coagulation pathway, and antigen processing and presentation pathway. The integration of pathways and eSNPs provides putative functional bridges between GWAS and candidate genes or pathways, thus serving as a potential powerful approach to identifying biological mechanisms underlying GWAS findings.

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confidence: 99%

Integrating Pathway Analysis and Genetics of Gene Expression for Genome-wide Association Studies

Zhong

Yang

Kaplan

et al. 2010

The American Journal of Human Genetics

222

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“…Kaneko et al [40] reported that TJ-41 markedly reduced extracellular concentration of NO at higher concentration in lipopolysaccharide-stimulated mouse macrophage-like RAW264.7 cells, while TJ-41 slightly enhanced NO at moderate concentration due to the co-existence of both the inhibitor and stimulator for NO production. In contrast, Liu et al [41] reported that TJ-41 increased NO in serum and pancreas tissue, leading to improve islet damage in diabetic rats. Taken together, the influence of TJ-41 on NO production may be dependent on dose of TJ-41, type of cells and tissues, and insults involved.…”

Section: Discussionmentioning

confidence: 90%

Japanese Herbal Medicine Hochuekkito Inhibits the Expression of Proinflammatory Biomarker, Inducible Nitric Oxide Synthase, in Hepatocytes

Matsumiya¹,

Kaibori²,

Araki³

et al. 2012

Med Chem

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Hochuekkito (TJ-41) is used for the treatment of complaints in patients with general fatigue. However, there is little scientific evidence to demonstrate the liver-protective effects of TJ-41. In the inflamed liver, proinflammatory cytokines stimulate the induction of inducible nitric oxide synthase (iNOS). Overproduction of NO by iNOS has been implicated as a factor in liver injury. We examined proinflammatory cytokine-stimulated hepatocytes as a simple in vitro injury model to determine liver-protective effects of TJ-41. The objective was to investigate whether TJ-41 influences iNOS induction and to determine its mechanism. Primary cultured rat hepatocytes were treated with interleukin (IL)-1β in the presence or absence of TJ-41. The induction of iNOS and its signaling pathway were analyzed. IL-1β produced increased levels of NO. This effect was inhibited by TJ-41, which exerted its maximal effects at 6 mg/ml. TJ-41 decreased the levels of iNOS protein and its mRNA expression. Experiments with nuclear extracts revealed that TJ-41 inhibited the translocation of NF-κB to the nucleus and its DNA binding. TJ-41 also inhibited the activation of Akt, resulting in the reduction of type I IL-1 receptor mRNA and protein expression. Transfection experiments demonstrated that TJ-41 suppressed iNOS induction by the inhibition of promoter transactivation and mRNA stabilization. TJ-41 reduced the expression of an iNOS gene antisense-transcript, which is involved in iNOS mRNA stability. Results indicate that TJ-41 inhibits the induction of iNOS at both transcriptional and post-transcriptional steps, leading to the prevention of NO production. TJ-41 may have therapeutic potential for various liver injuries through the suppression of iNOS induction.

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“…Three of the top 10 GO terms enriched for biological processes were associated with glucose transport and the synthesis, secretion, and action of insulin [ 46 – 48 ], suggesting a critical regulatory role for miR-27b in insulin-dependent glucose homeostasis. Moreover, gene targets for miR-27b were enriched in the protein kinase B (PKB) signalling and N-glycan biosynthesis pathways that have been associated with T2D [ 48 – 50 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Varies according to Glucose Tolerance, Measurement Platform, and Biological Source

Dias

Hemmings

Müller

et al. 2017

BioMed Research International

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Dysregulated microRNA (miRNA) expression is observed during type 2 diabetes (T2D), although the consistency of miRNA expression across measurement platform and biological source is uncertain. Here we report miRNA profiling in the whole blood and serum of South African women with different levels of glucose tolerance, using next generation sequencing (NGS) and quantitative real time PCR (qRT-PCR). Whole blood-derived miRNAs from women with newly diagnosed T2D (n = 4), impaired glucose tolerance (IGT) (n = 4), and normal glucose tolerance (NGT) (n = 4) were subjected to NGS, whereafter transcript levels of selected miRNAs were quantified in the whole blood and serum of these women using qRT-PCR. Of the five significantly differentially expressed miRNAs identified by NGS, only the directional increase of miR-27b in women with IGT compared to NGT was confirmed in whole blood and serum, using qRT-PCR. Functional enrichment of miR-27b gene targets identified biological pathways associated with glucose transport and insulin regulation. In conclusion, this study showed poor correlation in miRNA expression profiled using NGS and qRT-PCR and in whole blood and serum. The consistent increased expression of miR-27b in women with IGT compared to NGT across measurement platform and biological source holds potential as a biomarker for risk stratification in our population.

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Effect of Bu-Zhong-Yi-Qi-Tang on deficiency of N-glycan/nitric oxide and islet damage induced by streptozotocin indiabetic rats

Cited by 13 publications

References 21 publications

Integrating Pathway Analysis and Genetics of Gene Expression for Genome-wide Association Studies

Integrating Pathway Analysis and Genetics of Gene Expression for Genome-wide Association Studies

Japanese Herbal Medicine Hochuekkito Inhibits the Expression of Proinflammatory Biomarker, Inducible Nitric Oxide Synthase, in Hepatocytes

MicroRNA Expression Varies according to Glucose Tolerance, Measurement Platform, and Biological Source

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