Bilobalide abates inflammation, insulin resistance and secretion of angiogenic factors induced by hypoxia in 3T3-L1 adipocytes by controlling NF-κB and JNK activation

Priyanka, A; Sindhu, Ganapathy; Shyni, G. L.; Rani, Madhu; Nisha, V. M.; Raghu, Kozhiparambil Gopalan

doi:10.1016/j.intimp.2016.11.019

Cited by 40 publications

(28 citation statements)

References 59 publications

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“…The sudden ischemia leads to low oxygen supply and finally initiate cell death [25]. On the other side, increasing evidence demonstrated that bilobalide has significant effects on hypoxia-induced injury [26,27]. Our study employed OGD-stimulated H9c2 cells to build up MI cell The cardiomyocytes cells stimulated by OGD was often used to mimicked MI injury in vitro [28].…”

Section: Discussionmentioning

confidence: 97%

RETRACTED ARTICLE: Bilobalide protects H9c2 cell from oxygen-glucose-deprivation-caused damage via upregulation of miR-27a

Cao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Myocardial ischemia is a troublesome disease. Bilobalide possesses multiple biological functions. We researched the consequents of bilobalide in OGD-irritated H9c2 cells. Methods: OGD-stimulated H9c2 cells were treated by bilobalide, and/or transfected with miR-27a inhibitor or negative control. Use CCK-8 and flow cytometry to test cell activity and apoptosis, respectively. Luciferase activity experiment was to test targeting link between miR-27a and Tmub1. Levels of cell-cycle and apoptosis relative proteins and phosphorylation of PI3K/AKT and Wnt/b-catenin related proteins were detected through western blot. Results: OGD stimulation reduced cell activity and negatively regulated the expression of CDK4, CDK6 and CyclinD1. Cell apoptosis was increased and its related proteins were affected by OGD. Bilobalide administration reversed all the results above caused by OGD. OGD negatively regulated miR-27a while bilobalide upregulated miR-27a. miR-27a's target gene was Tmub1. The protection consequents of bilobalide were suppressed when cells were transfected with a miR-27a inhibitor that cell activity was reduced and apoptosis was raised. Attenuation in the phosphorylation level of PI3K, AKT and b-catenin by OGD was reversed by bilobalide, whereas there were opposite results after transfected with miR-27a inhibitor. Conclusion: Bilobalide relieved OGD-caused H9c2 cell damage, raising cell activity and attenuating apoptosis via upregulating miR-27a and activating of PI3K/AKT and Wnt/b-catenin signal pathway. HIGHLIGHTS 1. Bilobalide alleviates OGD-induced H9c2 cell injury. 2. Bilobalide upregulates miR-27a expression in OGD-stimulated H9c2 cells. 3. Bilobalide alleviates cell injury by upregulation of miR-27a. 4. Bilobalide actuates PI3K/AKT and Wnt/b-catenin pathways.

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Section: Discussionmentioning

confidence: 97%

RETRACTED ARTICLE: Bilobalide protects H9c2 cell from oxygen-glucose-deprivation-caused damage via upregulation of miR-27a

Cao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…It has however been shown that the deletion of hepatic prolyl hydroxylase domain enzyme 3 (PHD3) stabilizes the hypoxia-inducible factor-2 α (HIF-2 α ), a key factor of hypoxia responses, and improves insulin sensitivity [ 54 ] (see Stabilization and Destabilization of HIF-1 α ). As shown in Figure 1 , hypoxia results in increased inflammatory factors and free fatty acids that lead to insulin resistance via the activation of c-Jun amino-terminal kinase 1 (JNK-1) [ 55 ]. The activation of JNK-1 interferes with insulin signaling via phosphorylation of IRS-1 on serine 307 (Ser307) residue [ 56 , 57 ].…”

Section: Inflammation Of Obese Adipose Tissue and Insulin Resistanmentioning

confidence: 99%

“…Circulating levels of inflammatory factors including free fatty acids and TNF- α are higher in obesity [ 55 , 57 , 60 ]; these factors activate JNK-1, resulting in insulin resistance, as aforementioned [ 59 ]. It should be noted that TNF- α does not directly inhibit IRS-1.…”

Section: Inflammation Of Obese Adipose Tissue and Insulin Resistanmentioning

confidence: 99%

Hypoxia in Obesity and Diabetes: Potential Therapeutic Effects of Hyperoxia and Nitrate

Norouzirad

González‐Muniesa

Ghasemi

2017

Oxidative Medicine and Cellular Longevity

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The prevalence of obesity and diabetes is increasing worldwide. Obesity and diabetes are associated with oxidative stress, inflammation, endothelial dysfunction, insulin resistance, and glucose intolerance. Obesity, a chronic hypoxic state that is associated with decreased nitric oxide (NO) bioavailability, is one of the main causes of type 2 diabetes. The hypoxia-inducible factor-1α (HIF-1α) is involved in the regulation of several genes of the metabolic pathways including proinflammatory adipokines, endothelial NO synthase (eNOS), and insulin signaling components. It seems that adipose tissue hypoxia and NO-dependent vascular and cellular dysfunctions are responsible for other consequences linked to obesity-related disorders. Although hyperoxia could reverse hypoxic-related disorders, it increases the production of reactive oxygen species (ROS) and decreases the production of NO. Nitrate can restore NO depletion and has antioxidant properties, and recent data support the beneficial effects of nitrate therapy in obesity and diabetes. Although it seems reasonable to combine hyperoxia and nitrate treatments for managing obesity/diabetes, the combined effects have not been investigated yet. This review discusses some aspects of tissue oxygenation and the potential effects of hyperoxia and nitrate interventions on obesity/diabetes management. It can be proposed that concomitant use of hyperoxia and nitrate is justified for managing obesity and diabetes.

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“…What is more, the authors also demonstrated that the increase of vasorelaxation was notably declined by Nitric oxide inhibitor (Nishida & Satoh, ). In addition, BB was proved to function in declining inflammation, insulin resistance, and secretion of antigenic factors stimulated by hypoxia (Priyanka et al, ). Moreover, Zheng et al indicated that BB suppressed apoptosis, autophagy, and improved angiogenesis via AKT/endothelial nitric oxide synthase pathway (Zheng et al, ).…”

Section: Introductionmentioning

confidence: 99%

Retracted: Bilobalide alleviates tumor necrosis factor‐alpha‐induced pancreatic beta‐cell MIN6 apoptosis and dysfunction through upregulation of miR‐153

Hao

Wang

Wu³

et al. 2019

Phytotherapy Research

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Type 1 diabetes mellitus (T1DM) is a systemic disease and one classical type of total DM. Bilobalide (BB) is constituted of EGb 761. Our purpose was identifying the role of BB in TIDM in the current study. MIN6 cells were treated by TNF-α; then, viability, apoptosis, and insulin secretion were assessed by performing Cell Counting Kit-8 assay, flow cytometry, glucose-stimulated insulin secretion assay, and western blot.The effects of BB were assessed to identify its function. Further, the above mentioned parameters were reassessed when silencing miR-153. TNF-α declined viability and insulin secretion as well as raised apoptosis and inducible nitric oxide synthase (iNOS) expression in MIN6 cells. BB alleviated the apoptosis and dysfunction induced by TNF-α. MiR-153 expression was elevated by BB when induced by TNF-α. Increase of viability and insulin secretion as well as decline of apoptosis and iNOS induced by BB treatment was alleviated by silencing miR-153. The rates of p/t-p70S6K, p/tmammalian target of rapamycin (mTOR) and p/t-adenosine monophosphateactivated protein kinase (AMPK) were raised by BB and suppressed by silencing miR-153 under TNF-α induced condition. BB raised viability and insulin secretion, declined apoptosis and iNOS expression by up-regulating miR-153. Furthermore, BB activated AMPK/mTOR pathway by up-regulating miR-153.

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Bilobalide abates inflammation, insulin resistance and secretion of angiogenic factors induced by hypoxia in 3T3-L1 adipocytes by controlling NF-κB and JNK activation

Cited by 40 publications

References 59 publications

RETRACTED ARTICLE: Bilobalide protects H9c2 cell from oxygen-glucose-deprivation-caused damage via upregulation of miR-27a

RETRACTED ARTICLE: Bilobalide protects H9c2 cell from oxygen-glucose-deprivation-caused damage via upregulation of miR-27a

Hypoxia in Obesity and Diabetes: Potential Therapeutic Effects of Hyperoxia and Nitrate

Retracted: Bilobalide alleviates tumor necrosis factor‐alpha‐induced pancreatic beta‐cell MIN6 apoptosis and dysfunction through upregulation of miR‐153

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