Pioglitazone, a Peroxisome Proliferator-Activated Receptor γ Agonist, Ameliorates Chronic Kidney Disease by Enhancing Antioxidative Capacity and Attenuating Angiogenesis in the Kidney of a 5/6 Nephrectomized Rat Model

Sun, Li; Yuan, Quan; Xu, Tianhua; Li, Yao; Feng, Jingchun; Ma, Jun; Wang, Lining; Lu, Cuihua; Wang, Danan

doi:10.1159/000443121

Cited by 24 publications

(17 citation statements)

References 39 publications

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“…We also found that the antioxidant ability in the thigh muscle was improved with increased T‐AOC and GSH‐P X activity. Along with previous studies, which demonstrated that PGZ and rosiglitazone protected lipids against oxidative stress, we suggested that PGZ could function as an antioxidant to improve the meat quality of chickens. However, whether the effects of PGZ on improving meat quality are better than linoleic acids, daidzein, or other additives still needs further research.…”

Section: Discussionsupporting

confidence: 76%

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

et al. 2019

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BACKGROUND Muscle fat content and fatty acid composition play an important role in poultry flavor and taste. To investigate the effects of pioglitazone hydrochloride (PGZ) on growth performance and thigh muscle quality in yellow‐feathered chickens, 360 female chickens were randomly divided into three groups and treated with three doses of PGZ (0, 7.5, and 15 mg kg−1) for 28 days. Each group had six replicates of 20 chickens. RESULTS The results showed that dietary supplementation with 15 mg kg−1 PGZ increased average daily feed intake (ADFI) and the average daily gain (ADG) from 0 to 14 days. Furthermore, the triglyceride (TG) level was decreased by 15 mg kg−1 PGZ, whereas the eviscerated yield was increased. The relative weight of the heart and kidneys showed a linear increase with dietary PGZ supplementation, and the drip loss of the thigh muscle was significantly decreased by 15 mg kg−1 PGZ supplementation. Moreover, a* value, intramuscular fat (IMF), and polyunsaturated fatty acids (PUFAs) showed a linear increase, and pH24 h and drip loss showed a quadratic influence with the levels of PGZ supplementation. In particular, the PUFA proportion was increased by 7.63% and 9.14% in the 7.5 mg kg−1 PGZ and 15 mg kg−1 PGZ groups, respectively. Additionally, 15 mg kg−1 of PGZ increased the total antioxidant capacity (T‐AOC) and glutathione peroxidase (GSH‐PX) activity. CONCLUSION In summary, 15 mg kg−1 PGZ has substantial effects on growth performance and meat quality, particularly by decreasing drip loss and increasing IMF content, PUFA proportions, and antioxidant ability. © 2019 Society of Chemical Industry

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Section: Discussionsupporting

confidence: 76%

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

et al. 2019

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“…A negative correlation between the angiogenesis and intracellular ROS production has been proposed [10, 40]. Diabetes mellitus enhances the ROS, thus resulting in diminished NO bioavailability.…”

Section: Discussionmentioning

confidence: 99%

PPARα Agonist Stimulated Angiogenesis by Improving Endothelial Precursor Cell Function Via a NLRP3 Inflammasome Pathway

Deng¹,

Han²,

Zheng³

et al. 2017

Cell Physiol Biochem

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Background: Impaired wound healing is a common complication of diabetes and is the leading cause of lower extremity amputation. Treatment with fenofibrate, a peroxisome proliferators–activated receptor α (PPARα) agonist, was associated with a lower risk of amputations, particularly minor amputations without known large-vessel diseases, probably through non-lipid mechanisms. The current study aimed to test our hypothesis that fenofibrate stimulates angiogenesis and restores endothelial precursor cell (EPC) function via inhibiting Nod-like receptor protein 3 (NLRP3) inflammasome in streptozotocin (STZ)-induced diabetic mice. Methods: Male C57BL/6 mice were randomly divided into three groups: control, STZ-induced diabetic mice and fenofibrate treated diabetic group. Wound closure was assessed by wound area and CD31 positive capillaries. Both the migration and tube formation capacities of EPCs were measured. Intracellular nitric oxide (NO) and superoxide (O₂^-) levels were determined. Activity of NLRP3 inflammasome in EPCs was assessed by measuring thioredoxin-interacting protein (TXNIP), NLRP3, and caspase-1 expression. Results: Compared with the untreated diabetic mice, wound closure and capillary densities were significantly increased in fenofibrate treated group. Fenofibrate treatment restored EPC function, increased NO production, and decreased O₂^- level in EPCs of diabetic mice. Furthermore, fenofibrate deregulated the activity of NLRP3 inflammasome by reducing TXNIP, NLRP3 and caspase-1 expression in EPCs of diabetic mice. In vitro, fenofibrate prevented high glucose induced EPC dysfunction, deregulated NLRP3 inflammasome activity. In addition, fenofibrate inhibited IL-1β expression caused by combination use of high glucose and lipopolysaccharide. Conclusion: Fenofibrate can accelerate wound healing in diabetic mice, which at least in part was mediated by improving the impaired EPC function via a NLRP3 inflammasome pathway, suggesting the significance of PPARα agonists in the treatment of diabetes.

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“…I/R injury causes structural damage of renal tubules by directly inducing death of renal tubular cells, and these dying cells may release signals that trigger renal inflammatory responses [8][9][10][11][12][13][14]. The cross-talk of these complex pathways eventually initiates the development and progression of ARF.…”

Section: Introductionmentioning

confidence: 99%

MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis

Huang²,

梁英³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Ischemia/reperfusion injury (IRI) plays a crucial role in renal transplantation and can cause renal failure associated with pyroptosis, a pro-inflammatory-induced programmed cell death. Small endogenous non-coding RNAs have been shown to be involved in renal ischemia/reperfusion injury. This study was performed to investigate which miRNAs regulate pyroptosis in response to renal ischemia/reperfusion injury and determine the mechanism underlying this regulation. Methods: An in vivo rat model of renal IRI was established, and the serum and kidneys were harvested 24 h after reperfusion to assess renal function and histological changes. For the in vitro study, the cultured human renal proximal tubular cell line HK-2 was subjected to 24 h of hypoxia (5% CO₂, 1% O₂, and 94% N2) followed by 12 h of reoxygenation (5% CO₂, 21% O₂, and 74% N₂). The mRNA expression levels were analyzed by real-time PCR, and the protein expression levels were analyzed using Western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Bioinformatics analyses were applied to predict miR-155 targets, which were then confirmed by a luciferase reporter assay. Results: We found that the levels of pyroptosis-related proteins, including caspase-1, caspase-11, IL-1β and IL-18, were significantly increased after renal ischemia/reperfusion injury. Similarly, hypoxia-reoxygenation injury (HRI) also induced pyroptosis in HK2 cells. Furthermore, our study revealed that miR-155 expression was substantially increased in the renal tissues of IRI rats and in HRI HK2 cells. Up-regulation of miR-155 promoted HK2 cell pyroptosis in HRI; conversely, knockdown of miR-155 attenuated this process. To understand the signaling mechanisms underlying the pro-pyroptotic activity of miR-155, we found that exogenous expression of miR-155 up-regulated the expression of caspase-1 as well as the pro-inflammatory cytokines IL-1β and IL-18. Moreover, miR-155 directly repressed FoxO3a expression and its downstream protein apoptosis repressor with caspase recruitment domain (ARC). Conclusions: Our study proposes a new signaling pathway of miR-155/FoxO3a/ARC leading to renal pyroptosis under ischemia/reperfusion injury conditions.

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Pioglitazone, a Peroxisome Proliferator-Activated Receptor γ Agonist, Ameliorates Chronic Kidney Disease by Enhancing Antioxidative Capacity and Attenuating Angiogenesis in the Kidney of a 5/6 Nephrectomized Rat Model

Cited by 24 publications

References 39 publications

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

Dietary supplementation with pioglitazone hydrochloride improves intramuscular fat, fatty acid profile, and antioxidant ability of thigh muscle in yellow‐feathered chickens

PPARα Agonist Stimulated Angiogenesis by Improving Endothelial Precursor Cell Function Via a NLRP3 Inflammasome Pathway

MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis

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