scholarly journals Malaysian Bee Bread Attenuates Apoptosis and Improves Cell Proliferation in Testis of High-Fat Diet-Induced Obese Rats

Author(s):  
Joseph Bagi Suleiman ◽  
Ainul Bahiyah Abu Bakar ◽  
Mahaneem Mohamed

Introduction: Obesity has been reported to impair male reproductive function and testicular apoptosis while bee bread has been traditionally consumed to enhance male fertility.Objective: The objective of this study was to determine the effects of Malaysian bee bread on apoptosis and proliferation of testicular germ cells in high-fat diet-induced obese rats.Methods: Twenty-four adult male Sprague Dawley rats weighing between 250-300 g were randomised into four groups (n=6/group), namely normal control (NC), high-fat diet (HFD), HFD plus bee bread (HFD+B) and HFD plus an anti-obesity drug orlistat (HFD+O) groups. Bee bread (0.5g/kg/day) and orlistat (10 mg/kg/day) were suspended in distilled water and given by oral gavage for 12 weeks. Markers for apoptosis and proliferation of testicular germ cells were assessed.Results: mRNA transcript levels of caspase-3, caspase-8, caspase-9, p53 and Bax/Bcl2 ratio in the testis of HFD group were significantly increased while immunohistochemical staining of cleaved caspase-3 increased and proliferating cell nuclear antigen (PCNA) immunoexpress ions decreased relative to NC group. Treatment with bee bread significantly decreased the apoptotic markers, significantly decreased mRNA transcript levels of anti-apoptotic markers (Bcl2) and increased PCNA immunoexpression in HFD+B, relative to NC group and HFD+O.Conclusion: Bee bread improved proliferation of testicular germ cells by attenuating apoptosis in high- fat diet-induced obese male rats.International Journal of Human and Health Sciences Supplementary Issue: 2019 Page: 44

2012 ◽  
Vol 37 (6) ◽  
pp. 1101-1109 ◽  
Author(s):  
Marco Aurélio Aguiar e Silva ◽  
Ivan José Vechetti-Junior ◽  
André Ferreira do Nascimento ◽  
Kelly Silva Furtado ◽  
Luciana Azevedo ◽  
...  

The present study aimed to investigate the beneficial effects of swim training on the promotion–progression stages of rat liver carcinogenesis. Male Wistar rats were submitted to chemically induced liver carcinogenesis and allocated into 4 major groups, according their dietary regimen (16 weeks) and swim training of 5 days per week (8 weeks): 2 groups were fed low-fat diet (LFD, 6% fat) and trained or not trained and 2 groups were fed high-fat diet (HFD, 21% fat) and trained or not trained. At week 20, the animals were killed and liver samples were processed for histological analyses; immunohistochemical detection of persistent or remodeling preneoplastic lesions (pPNL and rPNL) expressing placental glutathione S-transferase (GST-P) enzyme; or proliferating cell nuclear antigen (PCNA), cleaved caspase-3, and bcl-2 protein levels by Western blotting or malonaldehyde (MDA) and total glutathione detection by HPLC. Overall analysis indicated that swim training reduced the body weight and body fat in both LFD and HFD groups, normalized total cholesterol levels in the HFD group while decreased the MDA levels, increased glutathione levels and both number of GST-P-positive pPNL and hepatocellular adenomas in LFD group. Also, a favorable balance in PCNA, cleaved caspase-3, and bcl-2 levels was detected in the liver from the LFD-trained group in relation to LFD-untrained group. The findings of this study indicate that the swim training protocol as a result of exercise postconditioning may attenuate liver carcinogenesis under an adequate dietary regimen with lowered fat intake.


2004 ◽  
Vol 91 (5) ◽  
pp. 715-723 ◽  
Author(s):  
Yajun Cheng ◽  
Lena Ohlsson ◽  
Rui-Dong Duan

Dietary fibre and fat affect colonic tumourigenesis and inflammation. Sphingomyelin metabolism may have implications for the pathogenesis of colonic tumours and ulcerative colitis. The present study examined the effects of psyllium and fat on the enzymes responsible for sphingomyelin metabolism and apoptosis in the colon. Mice were fed control, psyllium-containing (100 g/kg), high-fat (313 g/kg, 53 % energy as fat) or high-fat plus psyllium diets for 4 weeks. The activities of acid, neutral and alkaline sphingomyelinase (SMase), neutral ceramidase, and caspase 3, 8 and 9 in colonic mucosa were determined. The expressions of alkaline SMase and caspase 3 were examined. The psyllium-containing diet was found to increase significantly the activities of alkaline SMase and caspase 3 and decreased those of acid SMase and neutral ceramidase. The high-fat diet had opposite effects on these enzymes and attenuated the effects of psyllium. Western blotting showed that psyllium increased and high-fat decreased the levels of alkaline SMase and caspase 3 in colonic mucosa. The change in caspase 3 activity was positively correlated with that of alkaline SMase and negatively with acid SMase. No similar changes of acid and alkaline phosphatase activities in the colon or acid and neutral SMase activity in the liver were identified. In conclusion, colonic sphingomyelin metabolism and apoptosis were affected by psyllium and fat in an opposite manner. The results may have implications for colorectal tumourigenesis and inflammation.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Huadong Liu ◽  
Wei Xiong ◽  
Yu Luo ◽  
Hua Chen ◽  
Yaqiong He ◽  
...  

Background. Vascular remodeling is the most critical pathogenesis of atherosclerosis. Adipokine chemerin was known for its relationship with obesity as well as metabolism. Most recently, chemerin was found to play a crucial role in the pathologic process of cardiovascular diseases including coronary heart disease. In this study, we surveyed the role of chemerin in progression of atherosclerosis in ApoE−/− mice. Objective. To investigate the relationship between chemerin and progression of atherosclerosis in ApoE−/− mice and its mechanism. Methods. 8-week-old ApoE−/− mice were fed with high-fat diet to induce the atherosclerosis model. Adenoviruses were transfected for knockdown or overexpression of chemerin gene into aorta. Serums and aortic tissues of ApoE−/− mice were obtained after feeding high-fat diet for 16 weeks. HE staining and oil red staining were performed to evaluate aortic plaque. ELISA was performed to explore serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and transforming growth factor-β1 (TGF-β1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), proliferating cell nuclear antigen (PCNA), phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK 1/2). Result. Aortic plaque formation was significantly induced by high-fat diet in ApoE−/− mice. Simultaneously, elevated serum levels of TNF-α and IL-1β and elevated mRNA and protein levels of chemerin, NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 were found in ApoE−/− mice. After aortic chemerin gene was inhibited by adenovirus, aortic atherosclerosis induced by high-fat diet was significantly meliorated, serum levels of TNF-α and IL-1β decreased, mRNA and protein levels of NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 decreased simultaneously. Conclusion. Our study revealed that chemerin stimulated the progression of atherosclerosis in ApoE−/− mice.


2021 ◽  
Author(s):  
Luana Assis Ferreira ◽  
Fernando Victor Martins Rubatino ◽  
Mariana Lacerda de Freitas ◽  
Leonardo Rossi de Oliveira ◽  
Célio Jose de Castro Junior ◽  
...  

AbstractThe Rab3A and Rab3gaps are essential to the Ca+2-dependent neuronal exocytosis in the hypothalamus. The arcuate nucleus of the hypothalamus (ARC) controls food intake and energy expenditure. We have earlier described that the high-fat diet (HFD) feeding induces an obesity phenotype with high leptin production and alteration of proteins related to endosome sorting, and ubiquitination in the ARC of mice. In this study, real-time PCR data analysis revealed that HFD feeding decreases significantly Rab3a, Rab3gap1, and Rab3gap2 transcript levels in the ARC when compared to the group receiving a control diet. The decrease of Rab3gap1/2 transcript levels in the ARC was strongly associated with an increase in plasma leptin. Altogether, our studies demonstrate that HFD feeding could be altering the general network of endosome compartmentalization in the ARC of mice, contributing to a failure in exocytosis and receptor recycling.Graphical abstract


2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Zhang ◽  
Jie Ding ◽  
Yiru Wang ◽  
Xiaoteng Feng ◽  
Min Du ◽  
...  

Guanxinkang decoction (GXK), a traditional Chinese medicinal drug, is used to treat cardiovascular disease. The aim of the study was to investigate the effects of GXK on inflammation in LDLR−/− mice and RAW264.7 cells. Fed with high fat diet for 12 weeks, the mice were randomly divided into six groups, then administered with oral 0.9% saline or GXK (7.24, 14.48, and 28.96 g/kg) or Atorvastatin (1.3 mg/kg) for 12 weeks. RAW 264.7 cells were induced with ox-LDL or ox-LDL plus different concentrations of GXK (1.25, 2.5, and 5 μg/ml), or ox-LDL plus GXK plus MAPKs activators. Serum lipid profiles and inflammatory cytokines were detected by ELISA, gene expression by RT-qPCR, plaque sizes by Oil Red O, α-SMA, caspase 3, NF-κB p65 and TNF-α production by immunofluorescence staining, and protein expression by Western Blot. The phagocytic ability of cells was determined by neutral red uptake assay. Efferocytosis-related proteins (AML, MERTK, TYRO3 and MFGE8) and MAPKs pathways were detected by Western Blot. Compared to mice fed with high fat diet, the mice with GXK showed lower cholesterol, triglyceride, low-density lipoprotein cholesterol, IL-1β, IL-6, and TNF-α, smaller plaque sizes, higher α-SMA, and lower caspase 3 and NF-κB p65 in aortic roots. RAW264.7 cells treated with ox-LDL plus GXK had lower IL-1β, IL-6, and TNF-α. GXK also increased the phagocytic ability of cells. High levels of AML, MERTK, TYRO3 and MFGE8, and decreased levels of iNOS, VCAM-1, LOX-1 and MCP-1, and phosphorylation of ERK1/2, JNK, p38, and NF-κB were detected in GXK-treated group. MAPKs activators reversed the effects of GXK in repressing inflammation and promoting phagocytosis. These results suggested that GXK could attenuate atherosclerosis and resolve inflammation via efferocytosis and MAPKs signaling pathways in LDLR−/− mice and RAW264.7 cells.


2013 ◽  
Vol 217 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Sara Baldassano ◽  
Antonella Amato ◽  
Francesco Cappello ◽  
Francesca Rappa ◽  
Flavia Mulè

Endogenous glucagon-like peptide-2 (GLP2) is a key mediator of refeeding-induced and resection-induced intestinal adaptive growth. This study investigated the potential role of GLP2 in mediating the mucosal responses to a chronic high-fat diet (HFD). In this view, the murine small intestine adaptive response to a HFD was analyzed and a possible involvement of endogenous GLP2 was verified using GLP2 (3–33) as GLP2 receptor (GLP2R) antagonist. In comparison with animals fed a standard diet, mice fed a HFD for 14 weeks exhibited an increase in crypt–villus mean height (duodenum, 27.5±3.0%; jejunum, 36.5±2.9%;P<0.01), in the cell number per villus (duodenum, 28.4±2.2%; jejunum, 32.0±2.9%;P<0.01), and in Ki67-positive cell number per crypt. No change in the percent of caspase-3-positive cell in the villus–crypt was observed. The chronic exposure to a HFD also caused a significant increase in GLP2 plasma levels and in GLP2R intestinal expression. Daily administration of GLP2 (3–33) (30–60 ng) for 4 weeks did not modify the crypt–villus height in control mice. In HFD-fed mice, chronic treatment with GLP2 (3–33) reduced the increase in crypt–villus height and in the cell number per villus through reduction of cell proliferation and increase in apoptosis. This study provides the first experimental evidence for a role of endogenous GLP2 in the intestinal adaptation to HFD in obese mice and for a dysregulation of the GLP2/GLP2R system after a prolonged HFD.


Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1570
Author(s):  
Zuleyha Doganyigit ◽  
Birkan Yakan ◽  
Emin Kaymak

The aim of this project was the determination of the effect of bee bread supplement in diets of obese rats on interleukin 6 immunreactivity. This study has been shown that bee bread against obesity with a high-fat diet reduces IL-6 expression in the stomach.


Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 33 ◽  
Author(s):  
Zaidatul Akmal Othman ◽  
Wan Syaheedah Wan Ghazali ◽  
Liza Noordin ◽  
Nurul Aiman Mohd. Yusof ◽  
Mahaneem Mohamed

This study was undertaken to determine the phenolic compounds and the anti-atherogenic effect of bee bread in high-fat diet (HFD)-induced obese rats. The presence of phenolic compounds in bee bread was determined by liquid chromatography–mass spectrometry. Thirty-two male Sprague Dawley rats were divided into four groups, (n = 8/group); i.e., Normal (N), HFD (high-fat diet), HFD + BB (high-fat diet and 0.5 g/kg/day bee bread), and HFD + O (high-fat diet and 10 mg/kg/day orlistat) groups. After 6 weeks of the experiment, rats were sacrificed. Five phenolic compounds were identified in bee bread; namely, caffeic acid, ferulic acid, kaempferol, apigenin, and isorhamnetin. Bee bread significantly reduced Lee obesity index and levels of total cholesterol (TC), low-density lipoprotein (LDL), fatty acid synthase (FAS) activity, atherogenic index, oxidised-LDL (oxLDL), and malondialdehyde (MDA), and significantly increased aortic antioxidant activities, such as those of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Adipocyte sizes were found to be smaller in the HFD + BB group compared to the N group, and en face aortas showed an absence of atherosclerotic plaque in rats supplemented with bee bread. These changes might suggest an anti-atherogenic effect of bee bread in HFD-induced obese rats via its antioxidant and hypocholesterolaemic properties.


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