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Hypoglycemic Effects of Novel Panax notoginseng Polysaccharide in Mice with Diet-Induced Obesity.

ABSTRACT: In the study, the structural features and hypoglycemic effects of a polysaccharide Pan from the root of Panax notoginseng were investigated. The molecular weight of Pan was 8.27 kDa. Structural analysis indicated that Pan mainly consisted of →3)-β-L-Rhap-(1→, →3,6)-β-D-Galf-(1→ and →6)-β-D-Galf-(1→ residues with acetyl groups. Pan exhibited good antioxidant activity. Pan could slow down the body weight and the content of blood glucose in the high-fat diet-induced mice, further suppress GLUT-2 and SGLT-1 expression in the intestines, and enhance p-IRS and p-AMPK expression in the livers, finally exhibiting hypoglycemic effects. The results could supply a direction for further research on polysaccharides as components for the control of hyperglycemia induced by obesity and diabetes.

SUBMITTER: Li X

PROVIDER: S-EPMC9562645 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Hypoglycemic Effects of Novel Panax notoginseng Polysaccharide in Mice with Diet-Induced Obesity.

Li Xue X Liu Hao H Yang Hui-Rong HR Zeng Ying-Jie YJ

Foods (Basel, Switzerland) 20221005 19

In the study, the structural features and hypoglycemic effects of a polysaccharide Pan from the root of Panax notoginseng were investigated. The molecular weight of Pan was 8.27 kDa. Structural analysis indicated that Pan mainly consisted of →3)-β-L-Rhap-(1→, →3,6)-β-D-Galf-(1→ and →6)-β-D-Galf-(1→ residues with acetyl groups. Pan exhibited good antioxidant activity. Pan could slow down the body weight and the content of blood glucose in the high-fat diet-induced mice ...[more]

PMID: 36230175

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Project description:Background: Activation of the thermogenic program in white and brown adipocytes presents a promising avenue for increasing energy expenditure during the treatment of obesity. The endogenous mechanism for promoting thermogenesis in brown adipocytes or browning in white adipocytes has indicated that the gut microbiota is a crucial regulator of the host energy balance. However, whether the effects of the therapeutic intervention-induced modulation of the gut microbiota on adipocyte browning involved the regulation of leptin remains unclear. Method: The adipose features were analyzed by body composition analysis, infrared camera observations, transmission electron microscopy and H&E staining. The gene and protein expression in adipose tissue were detected by qRT-PCR, immunoblotting, immunohistochemistry and immunofluorescence staining. The gut microbiome signature was identified by 16S rRNA gene amplicon sequencing, and both mice with high-fat diet-induced obesity (DIO) and mice with antibiotics-induced microbiome depletion were subjected to fecal microbiota transplantation. Results: Treatment with Panax notoginseng saponins (PNS) shaped the murine gut microbiome by increasing the abundances of Akkermansia muciniphila and Parabacteroides distasonis, and as a result, DIO mice harbored a distal gut microbiota with a significantly increased capacity to reduce host adiposity. The PNS-induced modulation of the gut microbiota in DIO mice could increase brown adipose tissue (BAT) thermogenesis and beige adipocyte reconstruction by activating the leptin-AMPK/STAT3 signaling pathway, which results in the promotion of energy expenditure. Leptin has an essential influence on the anti-obesity effects of PNS. In cases of leptin deficiency, the PNS-induced modulation of the gut microbiota exerts negative effects on thermogenesis and browning in white adipose tissue (WAT), which indicates that PNS fail to reduce obesity in leptin gene-deficient mice. The PNS-induced modulation of the gut microbiota exerted a minimal effect on DIO mice with antibiotic-induced microbiome depletion, which confirmed the correlation between altered gut microbiota and the remodeling of adipose tissues in DIO mice. The direct influence of leptin on browning via the AMPKα/STAT3 signaling pathway in C3H101/2 cells supported our in vivo results that signalling through the leptin-AMPK/STAT3 pathway induced by the PNS-modulated gut microbiota was involved in beige adipocyte reconstruction. Conclusion: Our results revealed that leptin signaling is critical for alterations in microbiota-fat crosstalk and provide promising avenues for therapeutic intervention in the treatment of obesity.

Project description:Background: Community-associated methicillin-resistant staphylococcus aureus (CA-MRSA) is a drug-resistant bacterium prevalent in community settings, characterized by high pathogenicity and transmission potential. Polymorphonuclear neutrophils (PMNs) represent the first line of defense in innate immunity and are activated to phagocytose MRSA. However, MRSA, once phagocytosed by PMNs, induces necroptosis within the neutrophils, which is a key mechanism contributing to host damage.CA-MRSA releases virulence factors that enhance its pathogenicity by disrupting the host's innate immune response, particularly impairing the phagocytic function of PMNs. Steamed Panax notoginseng (S-PN) has demonstrated immune-regulatory and anti-inflammatory properties, showing promising therapeutic effects in alleviating the severe inflammatory responses induced by pathogenic microbial infections. Objective: This study aims to investigate the pharmacological effects and mechanisms of S-PN in attenuating CA-MRSA-induced necroptosis of PMNs, and to explore the impact of PMN necroptosis on the inflammatory response. Methods: A co-culture model of MRSA USA300 strain and PMNs isolated from healthy human blood was established to observe the changes in necroptosis marker HMGB1, PMNs counts, ROS, chemokine MCP-1 and pro-inflammatory cytokines IL-1β, IL-8, TNF-α. RNA-seq was employed to analyze the effects of S-PN on the transcriptional expression of pathogenesis-related genes of MRSA. RT-PCR was utilized to validate the expression of S-PN on MRSA virulence factors and PMNs necroptosis related genes. Results: S-PN significantly inhibited HMGB1, ROS, MCP-1, IL-1β and IL-8 in MRSA-PMN co-cultures, the PMN count in the S-PN group was higher than that in the model group. S-PN down-regulated MRSA pathogenic-associated Staphylococcus aureus infection and quorum sensing signaling pathways, and significantly reduced the virulence factors PSM and PVL. S-PN suppressed the expression of genes associated with necroptosis ripk1, ripk3, and mlkl in PMNs. Conclusion: S-PN inhibited CA-MRSA-induced necroptosis of PMNs, as well as the excessive inflammatory response and ROS accumulation accompanying this process. The mechanism involves the inhibition of the expression of MRSA virulence factor PSM and necroptosis pathway genes. These findings underscore the significant potential of S-PN in the treatment of CA-MRSA infections.

Dataset Information

Hypoglycemic Effects of Novel Panax notoginseng Polysaccharide in Mice with Diet-Induced Obesity.

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Hypoglycemic Effects of Novel <i>Panax notoginseng</i> Polysaccharide in Mice with Diet-Induced Obesity.

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