Fisetin ameliorates oxidative stress, inflammation and apoptosis in diabetic cardiomyopathy

Althunibat, Osama Y.; Hroob, Amir M. Al; Abukhalil, Mohammad H.; Germoush, Mousa O.; Bin-Jumah, May; Mahmoud, Ayman M.

doi:10.1016/j.lfs.2019.02.017

Cited by 126 publications

(96 citation statements)

References 64 publications

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“…To predict atherosclerosis and cardiovascular problems, the atherogenic indices (atherogenic index of plasma (AIP); atherogenic coefficient (AC); coronary risk index (CRI)) were calculated using the following equations [39][40][41]: Following anesthesia, excised inguinal fat was fixed by immersion in 4% formaldehyde in 0.1 M phosphate buffer overnight at 4 • C, washed inPBS, dehydrated in a graded series of ethanol, cleared in xylene, and embedded in paraffin. The paraffin blocks from each group were cut with a microtome into 5 µm thick sections, stained with hematoxylin and eosin (H&E), and inspected under a light microscope (×400, Olympus, Germany) equipped with a digital camera system (Carl Zeiss camera, model Axiocam ERc 5s.…”

Section: Measurement Of Lipid Profiles and Atherogenic Indicesmentioning

confidence: 99%

Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

et al. 2020

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Time-restricted feeding (TRF) showed a potent effect in preventing obesity and improving metabolicoutcomes in several animal models of obesity. However, there is, as of yet, scarce evidence concerning its effectiveness against obesogenic challenges that more accurately mimic human Western diets, such as the cafeteria diet. Moreover, the mechanism for its efficacy is poorly understood. White adipose browning has been linked to body weight loss. Herein, we tested whether TRF has the potential to induce browning of inguinal white adipose tissue (iWAT) and to attenuate obesity and associated dyslipidemia in a cafeteria-diet-induced obesity model. Male Wistar rats were fed normal laboratory chow (NC) or cafeteria diet (CAF) for 16 weeks and were subdivided into two groups that were subjected to either ad libitum (ad lib, A) or TRF (R) for 8 h per day. Rats under the TRF regimen had a lower body weight gain and adiposity than the diet-matchedad lib rats, despite equivalent levels of food intake and locomotor activity. In addition, TRF improved the deranged lipid profile (total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c)) and atherogenic indices (atherogenic index of plasma (AIP), atherogenic coefficient (AC), coronary risk index (CRI) in CAF-fed rats. Remarkably, TRF resulted in decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes in iWAT of NC- and CAF-fed rats. Protein expression of browning markers, such as uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were also up-regulated in the iWAToftime-restricted NC- or CAF-fed rats. These findings suggest that a TRF regimen is an effective strategy to improve CAF diet-induced obesity, probably via a mechanismthe involving WAT browning process.

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Section: Measurement Of Lipid Profiles and Atherogenic Indicesmentioning

confidence: 99%

Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

et al. 2020

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“…Excessive generation of ROS activates cytokines production, apoptotic proteins, and transcription factors, resulting in chronic inflammation and increased apoptosis, an underlying factor in the development of diabetic complications [1]. Evidence suggests that oxidative damage, pro-inflammatory responses, and apoptosis are key players in pathological conditions relating to diabetic cardiomyopathy [2,3]. Diabetic cardiomyopathy (DCM) is a pathological condition of the heart observed in subjects with diabetes, and it is independent of other cardiovascular pathologies such as hypertension, ischemic heart injury, coronary artery disease, and congenital heart diseases.…”

Section: Introductionmentioning

confidence: 99%

Effects of Anchomanes difformis on Inflammation, Apoptosis, and Organ Toxicity in STZ-Induced Diabetic Cardiomyopathy

et al. 2020

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Persistent hyperglycemia is known to cause enhanced generation of reactive oxygen species in diabetes. Several inflammatory cytokines are induced by oxidative stress, and their release also leads to increased oxidative stress; this makes oxidative stress one of the important factors in the development of chronic inflammation and other immune responses. These have been implicated in the development of diabetic complications such as nephropathy and cardiomyopathy. Anchomanes difformis has been shown to possess antioxidant and anti-inflammatory potentials. The present study investigated the immunomodulatory potential and the antiapoptotic ability of Anchomanes difformis to ameliorate heart toxicity and injury in type II diabetes. Two weeks of fructose (10%) administration followed by single intraperitoneal injection of streptozotocin (40 mg/kg) were used to induce type II diabetes in male Wistar rats. Leaf extract (aqueous) of Anchomanes difformis (200 and 400 mg/kg) was administered orally for six weeks. Blood glucose concentrations and body weights before and after interventions were determined. Interleukin (IL)-1β, IL-6, IL-10, IL-18, monocyte chemoattractant protein 1 (MCP-1), and tumor necrosis factor alpha (TNFα) were measured in the heart homogenates. Catalase (CAT), superoxide dismutase (SOD), total protein, oxygen radical absorbance capacity (ORAC), ferric reducing antioxidant power (FRAP), thiobarbituric acid reactive substances (TBARS), and heart-type fatty acid-binding protein (H-FABP) levels were determined. Expressions of transcription factors (Nrf 2 and NFkB/p65) and apoptotic markers were also investigated in the heart. Anchomanes difformis administration reduced pro-inflammatory cytokines, increased anti-inflammatory markers, and enhanced antioxidant defense in the heart of diabetic treated animals. Anchomanes difformis is a new, promising therapeutic agent that can be explored for the treatment of pathological conditions associated with immune responses and will be a useful tool in the management of associated diabetic complications.

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“…Previous studies have shown that FST has anti-tumor (Ferreira de Oliveira et al, 2018;Sun et al, 2018), anti-oxidation (Singh et al, 2018;Zhang et al, 2018), antiinflammatory Huang et al, 2018), and other pharmacological effects. It has been reported that FST inhibits inflammation related cytokines like TNF-a, IL-6, and NF-kB in streptozotocin (STZ)-induced diabetic cardiomyopathy rats (Althunibat et al, 2019). FST has also been shown to upregulate glutathione (GSH) in isoproterenol-induced cardiac ischemic injury rats and hyperhomocysteinemia-induced endothelial dysfunction rats (Hemanth Kumar et al, 2017;Garg et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Fisetin Prevents Acetaminophen-Induced Liver Injury by Promoting Autophagy

Zhang

Zhao

et al. 2020

Front. Pharmacol.

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Acetaminophen (APAP) overdose is a leading cause of drug-induced acute liver failure in clinical and hospital settings. Fisetin (FST) is a phenolic compound derived from natural products such as fruit and vegetables. Our research investigated the protective mechanisms of FST in APAP-induced hepatic injury in vitro and vivo. Assessment of mouse serum levels of alanine/aspartate aminotransferases (ALT/AST), liver myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) demonstrated the protective effects of FST toward APAP-induced liver injury. FST also reversed an APAP-induced decrease in mouse L-02 cell line viability. Our results also showed that FST significantly promoted APAPinduced autophagy and inhibited inflammasome activation both in vivo and in vitro. We also found that silencing ATG5, using si-ATG5, reduced the protective effects of FST against APAP-induced hepatotoxicity and reversed the effects on autophagy. Finally, we used the autophagy inhibitor, 3-methyladenine (3-MA) to validate the involvement of autophagy in FST against APAP-induced hepatotoxicity in vitro. We demonstrated that FST prevented APAP-induced hepatotoxicity by increasing ATG5 expression, thereby promoting autophagy and inhibiting inflammasome activation.

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Fisetin ameliorates oxidative stress, inflammation and apoptosis in diabetic cardiomyopathy

Cited by 126 publications

References 64 publications

Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

Effects of Anchomanes difformis on Inflammation, Apoptosis, and Organ Toxicity in STZ-Induced Diabetic Cardiomyopathy

Fisetin Prevents Acetaminophen-Induced Liver Injury by Promoting Autophagy

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