Role of PPARγ/Anti-inflammatory Axis in the Protective Effect of Ellagic Acid Against FSD/STZ-induced Gestational Diabetes in Rats

Abdel-Mone, Adel; Hosni, Ahmed; Abdel-Rehe, Eman Salah; Ismail, Amr

doi:10.3923/ajbs.2020.228.236

Cited by 5 publications

(22 citation statements)

References 21 publications

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“…35 In contrast, the level of adiponectin showed an effect on insulin sensitivity and its decreased level observed in the STZ induced GDM rats is related to the development of an insulin resistance state. 35 Treatment with nimbolide reduced leptin levels while increasing adiponectin levels, implying that insulin resistance was reduced. STZ induced apoptosis in pancreatic β-cells through DNA alkylation and the formation of harmful chemicals such as nitric oxide and superoxide anion, which further damaged the DNA and β-cell structure, resulting in apoptosis.. 37 In this study, we assessed the effect of STZ on histology, which revealed damage to pancreatic-cells as a result of diabetes, making the-cells unable to release insulin at physiological levels.…”

Section: Antioxidant Parametersmentioning

confidence: 88%

“…All these collectively take part in the pathogenesis of IR 35 . In contrast, the level of adiponectin showed an effect on insulin sensitivity and its decreased level observed in the STZ induced GDM rats is related to the development of an insulin resistance state 35 . Treatment with nimbolide reduced leptin levels while increasing adiponectin levels, implying that insulin resistance was reduced.…”

Section: Discussionmentioning

confidence: 98%

“…The current research showed an increased level of TNF‐α and leptin in the GDM group rats, which is strongly correlated with the expansion or progression of insulin resistance. The increased level of leptin in STZ induced GDM could be due to hyperleptinemia, which can lead to the development of leptin resistance, which can directly affect insulin resistance through a variety of mechanisms, including immune cell proliferation, IR tyrosine phosphorylation dysfunction, and increased peroxynitrite‐mediated oxidative stress 35 . All these mechanisms control the production of inflammatory cytokines, especially TNF‐α.…”

Section: Discussionmentioning

confidence: 99%

“…TNF‐α has been exhibited to arbitrate lipolysis, enhance FFA circulating and boost IR serine phosphorylation 36 . All these collectively take part in the pathogenesis of IR 35 . In contrast, the level of adiponectin showed an effect on insulin sensitivity and its decreased level observed in the STZ induced GDM rats is related to the development of an insulin resistance state 35 .…”

Section: Discussionmentioning

confidence: 99%

“…According to some published research, GDM is the early stage of T2DM, and insulin resistance is the shared pathophysiology of T2DM and GDM. 13,34 In this investigation, we treated GDM rats with nimbolide displayed a reduction in BGL and improved the level of 35 All these mechanisms control the production of inflammatory cytokines, especially TNF-α. TNF-α has been exhibited to arbitrate lipolysis, enhance FFA circulating and boost IR serine phosphorylation.…”

Section: Antioxidant Parametersmentioning

confidence: 96%

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Protective effect of nimbolide against streptozotocin induced gestational diabetes mellitus in rats via alteration of inflammatory reaction, oxidative stress, and gut microbiota

Meng

et al. 2022

Environmental Toxicology

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Background: Gestational diabetes mellitus (GDM) is a significant pregnancy-related condition, which showed effect on the development of fetal. Anti-inflammatory and antioxidant therapy commonly used for the treatment of GDM. Nimbolide already confirmed their anti-inflammatory and anti-oxidant effect against various animal disease model. Our objective in this research is to investigate the protective effect of nimbolide against STZ induced GDM and elucidate the mechanism.Methods: In this experimental study, pregnant female Wistar rats were used and STZ (40 mg/kg) was used to induce the GDM. Blood glucose level (BGL), body weight and plasma insulin were assessed at regular time (gestational day 0, 9, and 18). Water intake, food intake, fecal and urine output were also estimated. In the female rats, hemoglobin (Hb), glycalated hemoglobin (HbA1c), hepatic glycogen, fructosamine, adiponectin, leptin, lipid, antioxidant and inflammatory cytokines parameters were estimated. In the fetuses, the fetues weight, implementation loss, and fetal weight were estimated. At the completion of the protocol, biochemical parameters were calculated. Gut microbiota was estimated in end of the study. Results: Nimbolide treatment significantly (p < .001) improved the fetuses level and suppressed the fetal weight and implantation loss. Nimbolide treatment significantly (p < .001) suppressed the BGL and enhanced the body weight, insulin level. Nimbolide treatment suppressed the water intake, food intake, urinary and fecal output. Nimbolide significantly (p < .001) suppressed the fructosamine, leptin and enhanced the adiponectin level. Nimbolide treatment significantly (p < .001) decreased the malonaldehyde (MDA) level and boosted the total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione Stransferase (GST) and catalase (CAT); suppressed the level of TNF-α, IL-1β, IL-6, and boosted the level of IL-10. Furthermore, nimbolide treatment reversed the gut microbiota alteration induced via STZ in female rats. At the phylum level, the Firmicutes and Bacteroidetes relative abundance was altered via nimbolide treatment. The ratio of F/B boosted in GDM group and nimbolide treatment significantly (p < .001) suppressed. Nimbolide considerably suppressed the firmicutes and enhanced the Bacteroidetes, CAG-352, Lacnospirace.

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Section: Antioxidant Parametersmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%