Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Liu, Jinlei; Sun, Yao; Zheng, Hao; Wang, Jing; Liu, Huan; Song, Bing; Zhang, Haoqiang

doi:10.1155/2021/6662704

Cited by 3 publications

(1 citation statement)

References 44 publications

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“…38 Rheum officinale Baill can improve disorders of glucose-lipid metabolism and effectively treat DN by up-regulating the glucagon-like peptide-1 (GLP-1) receptor and decreasing the levels of TGF-β1 and α-SMA. 39 , 40 The addition of Astragalus mongholicus Bunge and Carthamus tinctorius L. to the formula targets the disease mechanism of qi deficiency and blood stasis. Astragalus mongholicus Bunge, being the most abundant component, replenishing qi to rise yang and abating fever.…”

Section: Discussionmentioning

confidence: 99%

Jiawei Shengjiangsan’s Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway

Yang,

Huang,

Fang

et al. 2024

DMSO

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Purpose This study aimed to investigate the intervention mechanism of Jiawei Shengjiangsan (JWSJS) on kidney injury in diabetic nephropathy mice. Methods Thirty 8-week-old db/db mice were randomly divided into five groups: model group, Perindopril group, and JWSJS low-, medium-, and high-dose groups (n=6 per group) based on body weight. Additionally, a blank control group was established consisting of 6 db/m mice aged 8 weeks. The blank and model groups received daily intragastric administration of 7g/kg/d pure water. The remaining groups were assigned to JWSJS low (3.5g/kg/d), medium (7g/kg/d), high (14g/kg/d) dosage groups, and perindopril positive control group (0.48mg/kg/d) for 12 weeks. Post-experiment, serum creatinine (SCr) and blood urea nitrogen (BUN) were analyzed using an automatic biochemical analyzer. Enzyme-linked immunosorbent assay (ELISA) measured 24-hour urinary albumin, neutrophil gelatinase-associated lipocalin (NGAL), TNF-α, IL-1β, VCAM-1, MCP-1, and HbA1c. Western blot assessed the protein expressions of p-PI3K, p-Akt, and p-NF-κB p65, while pathological kidney changes were observed. Results Compared to the blank group, the model group exhibited increased SCr, BUN, 24-hour urinary albumin, serum NGAL, TNF-α, IL-1β, VCAM-1, MCP-1, HbA1c, p-PI3K, and p-Akt, alongside increased p-NF-κB p65 expression, indicating significant kidney pathology. After treatment, the JWSJS group showed decreased SCr, BUN, 24-hour urinary microalbumin, NGAL, HbA1c, TNF-α, IL-1β, VCAM-1, MCP-1 levels, increased p-PI3K and p-Akt expression (P<0.05), and reduced p-NF-κB p65 content (P<0.05). Histopathological analysis revealed that JWSJS ameliorated renal tubular epithelial cell damage, glomerular capillary and basement membrane injuries, and facilitated the repair of damaged podocytes in diabetic nephropathy mice. Conclusion JWSJS demonstrated efficacy in reducing renal inflammation in diabetic nephropathy mice, with its mechanism likely associated with the inhibition of the PI3K/Akt/NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Jiawei Shengjiangsan’s Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway

Yang,

Huang,

Fang

et al. 2024

DMSO

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Emodin Alleviates High-Glucose-Induced Pancreatic β-Cell Pyroptosis by Inhibiting NLRP3/GSDMD Signaling

Xing

Zhang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Diabetes mellitus (DM) is a chronic noninfectious disease that is mainly featured by pancreatic β-cell (β-cell) dysfunction and impaired glucose homeostasis. Currently, the pathogenesis of dysfunction of the β-cells in DM remains unclear, and therapeutic approaches to it are limited. Emodin (EMD), a natural anthraquinone derivative, has been preliminarily proven to show antidiabetic effects. However, the underlying mechanism of EMD on β-cells still needs to be elucidated. In this study, we investigated the protective effects of EMD on the high glucose (50 mM)-induced INS-1 cell line and the underlying mechanism. INS-1 cells were treated with EMD (5, 10, and 20 μM) when exposed to high glucose. The effects of EMD were examined by using the inverted phase-contrast microscope, qRT-PCR, ELISA, and western blot. The results showed that EMD could alleviate cellular morphological changes, suppress IL-1β and LDH release, and promote insulin secretion in high-glucose-induced INS-1 cells. Furthermore, EMD inhibits NOD-like receptor protein 3 (NLRP3) activation and gasdermin D (GSDMD) cleavage to alleviate pyroptosis induced by high glucose. Overexpression of NLRP3 reversed the above changes caused by EMD. Collectively, our findings suggest that EMD attenuates high-glucose-induced β-cell pyroptosis by inhibiting NLRP3/GSDMD signaling.

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FPS-ZM1 attenuates the deposition of lipid in the liver of diabetic mice by sterol regulatory element binding protein-1c

Zhang,

Zhao,

Zhang

et al. 2024

BMC Endocr Disord

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Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

Cited by 3 publications

References 44 publications

Jiawei Shengjiangsan’s Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway

Jiawei Shengjiangsan’s Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway

Emodin Alleviates High-Glucose-Induced Pancreatic β-Cell Pyroptosis by Inhibiting NLRP3/GSDMD Signaling

FPS-ZM1 attenuates the deposition of lipid in the liver of diabetic mice by sterol regulatory element binding protein-1c

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