Celastrol suppresses obesity process via increasing antioxidant capacity and improving lipid metabolism

Wang, Chaoyun; Shi, Chunfeng; Yang, Xiaoping; Yang, Ming; Sun, Hongliu; Wang, Chunhua

doi:10.1016/j.ejphar.2014.09.043

Cited by 80 publications

(48 citation statements)

References 34 publications

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“…To date, celastrol has been widely used for the treatment of various diseases, such as cancer, neurodegenerative disease, and autoimmune diseases [ 12 – 15 ]. The latest research reported that celastrol was able to effectively alleviate high-fat mediated cardiovascular disease and diabetic nephropathy [ 16 , 17 ]. But there is still a lack of data describing the anti-inflammatory and immunosuppressive activities of celastrol on diabetic liver injury.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

Han

Sun

et al. 2016

Journal of Diabetes Research

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Immune and inflammatory pathways play a central role in the pathogenesis of diabetic liver injury. Celastrol is a potent immunosuppressive and anti-inflammatory agent. So far, there is no evidence regarding the mechanism of innate immune alterations of celastrol on diabetic liver injury in type 2 diabetic animal models. The present study was aimed at investigating protective effects of celastrol on the liver injury in diabetic rats and at elucidating the possible involved mechanisms. We analyzed the liver histopathological and biochemical changes and the expressions of TLR4 mediated signaling pathway. Compared to the normal control group, diabetic rats were found to have obvious steatohepatitis and proinflammatory cytokine activities were significantly upregulated. Celastrol-treated diabetic rats show reduced hepatic inflammation and macrophages infiltration. The expressions of TLR4, MyD88, NF-κB, and downstream inflammatory factors IL-1β and TNFα in the hepatic tissue of treated rats were downregulated in a dose-dependent manner. We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-κB signaling cascade pathways and its downstream inflammatory effectors.

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Section: Introductionmentioning

confidence: 99%

Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

Han

Sun

et al. 2016

Journal of Diabetes Research

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“…To understand the antifungal activity of the quinonemethide, the ROS dependent gene expressions in C. neoformans were measured owing to their known antioxidative activity (Allison et al 2001, Wang et al 2014. Because terpenoids are known to induce an increase in intracellular ROS, we selected genes encoding antioxidant proteins, sod1 and sod2, for the superoxide dismutases that convert superoxide radical to hydrogen peroxide, and ccp1, for the cytochrome c peroxidase that detoxifies hydrogen peroxide (Cox et al 2003;Narasipura et al 2003;Giles et al 2005;Narasipura et al 2005).…”

Section: Resultsmentioning

confidence: 99%

Downregulation of fungal cytochrome c peroxidase expression by antifungal quinonemethide triterpenoids

Seo

Lee

Park

et al. 2016

Journal of Applied Biological Chemistry

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To handle the development of antifungal drug resistance, the development of new structural modules and new modes of action for antifungals have been highlighted recently. Here, the antifungal activity of quinonemethidal triterpenoids such as celastrol, dihydrocelastrol, iguestein, pristimerin, and tingenone isolated from Tripterygium regelii were identified (MIC 0.269-19.02 µM). C. glabrata was the most susceptible to quinonemethide among the tested fungi. Furthermore, quinonemethide suppressed cyctochrome c peroxidase expression dramatically, decreasing fungal viability caused by the accumulation of hydrogen peroxide. Thus, cyctochrome c peroxidase downregulation of quinonemethide may be a key mode of action for antifungals.

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“…Of high clinical importance, recent observations indicate that some specific antioxidants by suppression of oxidative stress can prevent accumulation of “bad” adipose tissue and weight gain. Celastrol, triterpenoid compounds with antioxidant and anti-inflammatory properties, was able to effectively suppress weight and alleviate high-fat mediated cardiovascular injury via mitigating oxidative stress and improving lipid metabolism [188] . Also, α-lipoic acid increased mitochondrial content, enhanced oxygen consumption and fatty acid oxidation enzymes in cultured white subcutaneous adipocytes from overweight/obese donors [189] .…”

Section: Conclusion and Clinical Implicationmentioning

confidence: 99%

Redox implications in adipose tissue (dys)function—A new look at old acquaintances

et al. 2015

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Obesity is an energy balance disorder associated with dyslipidemia, insulin resistance and diabetes type 2, also summarized with the term metabolic syndrome or syndrome X. Increasing evidence points to “adipocyte dysfunction”, rather than fat mass accretion per se, as the key pathophysiological factor for metabolic complications in obesity. The dysfunctional fat tissue in obesity characterizes a failure to safely store metabolic substrates into existing hypertrophied adipocytes and/or into new preadipocytes recruited for differentiation. In this review we briefly summarize the potential of redox imbalance in fat tissue as an instigator of adipocyte dysfunction in obesity. We reveal the challenge of the adipose redox changes, insights in the regulation of healthy expansion of adipose tissue and its reduction, leading to glucose and lipids overflow.

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Celastrol suppresses obesity process via increasing antioxidant capacity and improving lipid metabolism

Cited by 80 publications

References 34 publications

Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

Downregulation of fungal cytochrome c peroxidase expression by antifungal quinonemethide triterpenoids

Redox implications in adipose tissue (dys)function—A new look at old acquaintances

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