Dataset Information

Effects of polysaccharides-riched Prunus mume fruit juice concentrate on uric acid excretion and gut microbiota in mice with adenine-induced chronic kidney disease.

ABSTRACT: The present study aimed to determine the effects of polysaccharides-riched Prunus mume fruit juice concentrate (PFC) on uric acid (UA) excretion and the gut microbiota in mice with chronic kidney disease (CKD). C57BL/6 mice were randomly allocated to four groups: two that were fed AIN93M diet, one of which was administered 500 mg/kg PFC, and two that were fed AIN93M diet containing 0.2% adenine, one of which was administered 500 mg/kg PFC. PFC promoted UA excretion, which may have been mediated through increases in the protein expression of ATP-binding cassette transporter G2 (ABCG2), organic anion transporter 1 (OAT1), organic carnitine transporter 2 (OCTN2), and reductions in the protein expression of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in kidneys of CKD mice. ABCG2 expression in the intestine was also increased by PFC administration. Additionally, PFC significantly increased large intestinal short-chain fatty acids (SCFAs) concentrations, and the number of gut microbial species, and reduced the abundance of the genera Bacteroides, Pseudoflavonifractor, Helicobacter, Clostridium_IV and Allobaculum, which have a negative effect on UA excretion. In conclusion, PFC may promote UA excretion in CKD mice by altering the expression of urate transporters and regulating the gut microbiota.

SUBMITTER: Huang Y

PROVIDER: S-EPMC9649360 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Effects of polysaccharides-riched <i>Prunus mume</i> fruit juice concentrate on uric acid excretion and gut microbiota in mice with adenine-induced chronic kidney disease.

Huang Yan Y Wu Chen-Xi CX Guo Lu L Zhang Xiao-Xi XX Xia Dao-Zong DZ

Current research in food science 20221031

The present study aimed to determine the effects of polysaccharides-riched <i>Prunus mume</i> fruit juice concentrate (PFC) on uric acid (UA) excretion and the gut microbiota in mice with chronic kidney disease (CKD). C57BL/6 mice were randomly allocated to four groups: two that were fed AIN93M diet, one of which was administered 500 mg/kg PFC, and two that were fed AIN93M diet containing 0.2% adenine, one of which was administered 500 mg/kg PFC. PFC promoted UA excretion, which may have been me ...[more]

PMID: 36387593

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Project description:Bud dormancy is a critical developmental process for perennial plant survival, and also an important physiological phase that affects the next season’s growth of temperate fruit trees. Bud dormancy is regulated by multiple genetic factors, and affected by various environmental factors, tree age and vigor. To understand molecular mechanism of bud dormancy in Japanese apricot (Prunus mume Sieb. et Zucc.), we constructed a custom oligo DNA microarray covering the Japanese apricot dormant bud ESTs referring to peach (P. persica) genome sequence. Because endodormancy release is a chilling temperature-dependent physiological event, genes showing chilling-mediated differential expression patterns are candidates to control endodormancy release. Using the microarray constructed in this study, we monitored gene expression changes of dormant vegetative buds of Japanese apricot during prolonged artificial chilling exposure. In addition, we analyzed seasonal gene expression changes. ‘Nanko’ vegetative buds collected in November, and those exposed to chilling for 40 or 60 days were used as microarray samples. Among the 58539 different unigene probes, 2345 and 1059 genes were identified as being more than two-fold up-regulated and down-regulated, respectively, following chilling exposure for 60 days (P value < 0.05). The down-regulated genes included P. mume DORMANCY-ASSOCIATED MADS-box genes, which supported the previous quantitative RT-PCR and EST analyses showing that these genes are repressed by prolonged chilling treatments. The genes encoding lipoxygenase were remarkably up-regulated by prolonged chilling. Cluster analysis suggested that the expression of the genes showing expression changes by artificial chilling exposure were coordinately regulated by seasonal changes. Our parametric analysis of gene set enrichment suggested that genes related to jasmonic acid (JA) and oxylipin biosynthesis and metabolic processes were significantly up-regulated by prolonged chilling, whereas genes related to circadian rhythm were significantly down-regulated. The results obtained from the microarray analyses were verified by quantitative RT-PCR analysis of selected genes. Taken together, this study raised the possibility that the microarray platform constructed in this study is applicable for deeper understanding of molecular network related to agronomically important bud phisiologies including dormancy release.

Project description:Bud dormancy is a critical developmental process for perennial plant survival, and also an important physiological phase that affects the next seasonM-bM-^@M-^Ys growth of temperate fruit trees. Bud dormancy is regulated by multiple genetic factors, and affected by various environmental factors, tree age and vigor. To understand molecular mechanism of bud dormancy in Japanese apricot (Prunus mume Sieb. et Zucc.), we constructed a custom oligo DNA microarray covering the Japanese apricot dormant bud ESTs referring to peach (P. persica) genome sequence. Because endodormancy release is a chilling temperature-dependent physiological event, genes showing chilling-mediated differential expression patterns are candidates to control endodormancy release. Using the microarray constructed in this study, we monitored gene expression changes of dormant vegetative buds of Japanese apricot during prolonged artificial chilling exposure. In addition, we analyzed seasonal gene expression changes. M-bM-^@M-^XNankoM-bM-^@M-^Y vegetative buds collected in November, and those exposed to chilling for 40 or 60 days were used as microarray samples. Among the 58539 different unigene probes, 2345 and 1059 genes were identified as being more than two-fold up-regulated and down-regulated, respectively, following chilling exposure for 60 days (P value < 0.05). The down-regulated genes included P. mume DORMANCY-ASSOCIATED MADS-box genes, which supported the previous quantitative RT-PCR and EST analyses showing that these genes are repressed by prolonged chilling treatments. The genes encoding lipoxygenase were remarkably up-regulated by prolonged chilling. Cluster analysis suggested that the expression of the genes showing expression changes by artificial chilling exposure were coordinately regulated by seasonal changes. Our parametric analysis of gene set enrichment suggested that genes related to jasmonic acid (JA) and oxylipin biosynthesis and metabolic processes were significantly up-regulated by prolonged chilling, whereas genes related to circadian rhythm were significantly down-regulated. The results obtained from the microarray analyses were verified by quantitative RT-PCR analysis of selected genes. Taken together, this study raised the possibility that the microarray platform constructed in this study is applicable for deeper understanding of molecular network related to agronomically important bud phisiologies including dormancy release. In this study, we used chilling exposed bud samples (0, 40, 60 days starting at November) and seasonal monthly bud samples (June to March). For the samples in dataset 1 (three different time points during chilling treatment), three technical replicates (60K M-CM-^W 3 per sample) with three biological replicates were averaged, whereas three technical replicates were averaged for the samples in dataset 2 (10 different seasonal time points)

Dataset Information

Effects of polysaccharides-riched Prunus mume fruit juice concentrate on uric acid excretion and gut microbiota in mice with adenine-induced chronic kidney disease.

Publications

Effects of polysaccharides-riched <i>Prunus mume</i> fruit juice concentrate on uric acid excretion and gut microbiota in mice with adenine-induced chronic kidney disease.

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