Anti-hyperuricemic potential of stevia (<i>Stevia rebaudiana</i>Bertoni) residue extract in hyperuricemic mice

Mehmood, Arshad; Zhao, Liang; Ishaq, Muhammad; Wang, Xin; Zhao, Lei; Hossen, Imam; Zhang, Huimin; Lian, Yunhe; Xu, Meili

doi:10.1039/c9fo02246e

Cited by 43 publications

(52 citation statements)

References 86 publications

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“…SAL significantly increased the activities of the antioxidant enzymes, including SOD, CAT, and GSH, and also suppressed the production of ROS and MDA. These results are in line with many studies (Hong et al, 2014;Wang et al, 2016;Mehmood et al, 2020). In addition, 200 mg/kg of SAL has a stronger effect on CAT, GSH activity, and MDA level than BZM, and its ameliorative effect on GSH activity is better than that of FBX.…”

Section: Discussionsupporting

confidence: 91%

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The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

Chen

Jiang

et al. 2021

Front. Pharmacol.

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Sonneratia apetala Buch-Ham., an exotic mangrove species with antidiabetic, antibacterial, and antioxidant capacities, mainly distributes in the southeast coastal areas in China. The present work investigated the protective effects of Sonneratia apetala leaves and branches extraction (SAL) on hyperuricemia (HUA) in mice. Potassium oxonate (PO) and hypoxanthine (HX) were used to establish the HUA model by challenge for consecutive 7 days. Results revealed that SAL inhibited the increases in kidney weight and index compared to the vehicle group. Meanwhile, SAL significantly decreased the levels of uric acid (UA), creatinine (CRE), and blood urea nitrogen (BUN) in serum. Additionally, SAL inhibited the activity of xanthine oxidase (XOD) in the liver. SAL ameliorated PO- and HX-induced histopathological changes. Moreover, it regulated oxidative stress markers including malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) activity, and glutathione (GSH) content. Also, SAL inhibited the increases in renal levels of interleukin-6 (IL-6), interleukin-18 (IL-18), interleukin-1β (IL-1β), tumor necrosis factor (TNF-α), monocyte chemotactic protein 1 (MCP-1), and transforming growth factor-β (TGF-β). SAL remarkably reduced suppressor of cytokine signaling 3 (SOCS3), Janus kinase 2 (JAK2), and subsequent phosphorylation of signal transducer and activator of transcription 3 (STAT3) expression. In addition, SAL inhibited the activation of nuclear factor kappa-B (NF-κB) in the kidney. Furthermore, SAL protected against HUA by regulating renal UA transporters of organic anion transporter (OAT1), urate reabsorption transporter 1 (URAT1), and glucose transporter 9 (GLUT9). These findings suggested that SAL ameliorated HUA by inhibiting the production of uric acid and enhancing renal urate excretion, which are related to oxidative stress and inflammation, and the possible molecular mechanisms include its ability to inhibit the JAK/STAT signaling pathway. Thus, SAL might be developed into a promising agent for HUA treatments.

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Section: Discussionsupporting

confidence: 91%

“…Accumulation of UA triggers renal injury by production of pro-inflammatory cytokines. Besides, oxidative stress can also aggravate the inflammatory responses via activation of the NF-κB pathway (Mehmood et al, 2020). Thus, the effect against the activation of the NF-κB pathway might be related to the antioxidant activity.…”

Section: Discussionmentioning

confidence: 99%

The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

Chen

Jiang

et al. 2021

Front. Pharmacol.

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“…It has been reported that iptakalim, an ATPsensitive potassium channel opener, could improve endothelial dysfunction and defend against hyperuricemia [86]. And using stevia (Stevia rebaudiana Bertoni) byproduct, named stevia residue extract (STVRE), to treat hyperuricemia, Arshad Mehmood et al confirmed in a recent study that the STVRE remarkably attenuated oxidative stress mediated by UA and downregulated inflammatory-related response markers such as COX-2, NF-κB, PGE2, IL-1β, and TNF-α [87]. In addition, related research has shown that UAinduced oxidative stress may activate the Notch 1 pathway, which is involved in the UA inflammatory process.…”

Section: Oxidative Stress and Endothelial Dysfunction Inmentioning

confidence: 99%

The Role of Oxidative Stress in Hyperuricemia and Xanthine Oxidoreductase (XOR) Inhibitors

Liu

Sun

et al. 2021

Oxidative Medicine and Cellular Longevity

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Uric acid is the end product of purine metabolism in humans. Hyperuricemia is a metabolic disease caused by the increased formation or reduced excretion of serum uric acid (SUA). Alterations in SUA homeostasis have been linked to a number of diseases, and hyperuricemia is the major etiologic factor of gout and has been correlated with metabolic syndrome, cardiovascular disease, diabetes, hypertension, and renal disease. Oxidative stress is usually defined as an imbalance between free radicals and antioxidants in our body and is considered to be one of the main causes of cell damage and the development of disease. Studies have demonstrated that hyperuricemia is closely related to the generation of reactive oxygen species (ROS). In the human body, xanthine oxidoreductase (XOR) catalyzes the oxidative hydroxylation of hypoxanthine to xanthine to uric acid, with the accompanying production of ROS. Therefore, XOR is considered a drug target for the treatment of hyperuricemia and gout. In this review, we discuss the mechanisms of uric acid transport and the development of hyperuricemia, emphasizing the role of oxidative stress in the occurrence and development of hyperuricemia. We also summarize recent advances and new discoveries in XOR inhibitors.

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“…Uric acid promotes the activation of platelet-derived growth factor receptor-β (PDGFR-β) through the p38 MAPK and ERK1/2 pathways, thereby inducing and aggravating cardiovascular diseases [29]. In a hyperuricemia animal model, uric acid can upregulate the expression of inflammatory factors such as cyclooxygenase-2 (COX-2), IL-1β, and TNF-α and play an important role in the development of complications related to hyperuricemia [30].…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology-Based Investigation of the Mechanism of Action of Plantaginis Herba in Hyperuricemia Treatment

Tang

Peng

Wang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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This study used a network pharmacology approach to investigate the potential active ingredients of Plantaginis Herba and its underlying mechanisms in hyperuricemia treatment. The potential active ingredients of Plantaginis Herba were obtained from TCMSP and ETCM databases, and the potential targets of the active ingredients were predicted using the Swiss TargetPrediction database. The potential therapeutic targets of hyperuricemia were retrieved from the GeneCards, DisGeNET, and Online Mendelian Inheritance in Man (OMIM) databases. Then, the integrative bioinformatics analyses of candidates were performed by GO analysis, KEGG analysis, and PPI network construction. There were 15 predicted active ingredients in Plantaginis Herba and 41 common targets that may be involved in the treatment of hyperuricemia. A total of 61 GO annotations and 35 signaling pathways were identified by enrichment analysis ( P < 0.01 ). The underlying mechanisms of Plantaginis Herba may be related to insulin resistance, PI3K/AKT, TNF, VEGF, AMPK, and glucagon signaling pathways. Thus, the present study provided potential and promising strategies of Plantaginis Herba for hyperuricemia treatment.

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Anti-hyperuricemic potential of stevia (Stevia rebaudianaBertoni) residue extract in hyperuricemic mice

Abstract:
STVRE has strong potential in combating HUA through following possible mechanisms; (1), inhibited XOD enzyme (2), exhibited uricosuric effect, (3) improved UA mediated oxidative stress, (4) remarkably reduced renal inflammation caused by UA.

Cited by 43 publications

References 86 publications

The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

The Role of Oxidative Stress in Hyperuricemia and Xanthine Oxidoreductase (XOR) Inhibitors

Network Pharmacology-Based Investigation of the Mechanism of Action of Plantaginis Herba in Hyperuricemia Treatment

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Anti-hyperuricemic potential of stevia (Stevia rebaudianaBertoni) residue extract in hyperuricemic mice

Abstract: STVRE has strong potential in combating HUA through following possible mechanisms; (1), inhibited XOD enzyme (2), exhibited uricosuric effect, (3) improved UA mediated oxidative stress, (4) remarkably reduced renal inflammation caused by UA.

Cited by 43 publications

References 86 publications

The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

The Extract of Sonneratia apetala Leaves and Branches Ameliorates Hyperuricemia in Mice by Regulating Renal Uric Acid Transporters and Suppressing the Activation of the JAK/STAT Signaling Pathway

The Role of Oxidative Stress in Hyperuricemia and Xanthine Oxidoreductase (XOR) Inhibitors

Network Pharmacology-Based Investigation of the Mechanism of Action of Plantaginis Herba in Hyperuricemia Treatment

Contact Info

Product

Resources

About

Abstract:
STVRE has strong potential in combating HUA through following possible mechanisms; (1), inhibited XOD enzyme (2), exhibited uricosuric effect, (3) improved UA mediated oxidative stress, (4) remarkably reduced renal inflammation caused by UA.