scholarly journals Hyperbilirubinemia Reduces the Streptozotocin-Induced Pancreatic Damage through Attenuating the Oxidative Stress in the Gunn Rat

2010 ◽  
Vol 222 (4) ◽  
pp. 265-273 ◽  
Author(s):  
Yan Yan Fu ◽  
Kyung Ja Kang ◽  
Jung Myung Ahn ◽  
Hae-Ryoung Kim ◽  
Ki Young Na ◽  
...  
Metabolism ◽  
2008 ◽  
Vol 57 (9) ◽  
pp. 1253-1261 ◽  
Author(s):  
Seonghun Ryu ◽  
Asher Ornoy ◽  
Amram Samuni ◽  
Sarah Zangen ◽  
Ron Kohen

Author(s):  
Rizgar Khalid Nabi ◽  
Mahdi Ali Abdullah

Background: Diabetes is directly involved in oxidative stress production. Therefore, this work was conducted to investigate the histopathological changes which occur in parenchymatous and to evaluate the antioxidant effect of quercetin in alloxan induced diabetes in male albino rats.Methods: Thirty-six male albino rats were divided into six groups of 6 rats in each group and treated as follows: a control group, quercetin group, diabetic control group, diabetic with quercetin group, diabetic with insulin group, diabetic with quercetin plus insulin group, alloxan was administered as a single dose (140 mg/kg body weight) to induce diabetes.Results: Result showed histopathological changes which included degenerative to necrotic changes of the liver, kidney and pancreas and this are due to the effect of oxidative stress that occurred from diabetes by alloxan. Conversely, quercetin significantly modulated improved histopathological changes founded on this study with or without of insulin, furthermore, results showed that damaged tissues where improved when groups of rats treated with quercetin and insulin together.Conclusions: It has been concluded that the quercetin could be promising antioxidants for reducing the risk of oxidation induced by diabetes that lead to nephrotoxicity, hepatotoxicity and pancreatic damage.


Author(s):  
Chan Hum Park ◽  
Joo Young Lee ◽  
Sung Ho Shin ◽  
Min Yeong Kim ◽  
Eun Suk Lee ◽  
...  

Oligonol is a low-molecular-weight polyphenol derived from lychee fruit. This study was conducted to examine whether oligonol has an ameliorative effect on diabetes-induced pancreatic damage via oxidative stress-induced inflammation. Oligonol was orally administered at 10 or 20 mg/kg body weight/day for 10 days to streptozotocin-induced diabetic rats, and changes in serum glucose, C-peptide, insulin, reactive oxygen species (ROS), and thiobarbituric acid-reactive substance (TBARS) levels as well as body weight and food and water consumption were assessed. Furthermore, rat pancreases were analyzed for weight, ROS generation, TBARS level, insulin content, and protein expressions of phosphor (p)-p38, p-extracellular-signal regulated kinase 1/2, p-inhibitor of nuclear factor kappa Bα, nuclear factor-kappa Bp65, cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6. Markers of diabetes were shown to be decreased by oligonol administration and histological damage in the pancreas was also ameliorated. These results indicate that oligonol exerts antidiabetic activities, which may be mediated via antioxidative, stress-related, anti-inflammatory signaling.


2015 ◽  
Vol 91 (7) ◽  
pp. 381-385 ◽  
Author(s):  
Yumiko Uchida ◽  
Yukihiro Morimoto ◽  
Takao Uchiike ◽  
Tomoyuki Kamamoto ◽  
Tamaki Hayashi ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jiyan Yuan ◽  
Zeliang Wei ◽  
Guang Xin ◽  
Xubao Liu ◽  
Zongguang Zhou ◽  
...  

Acute pancreatitis is an inflammatory disorder of the pancreas associated with substantial morbidity and mortality, which is characterized by a rapid depletion of glutathione (GSH). Cysthionine-β-synthase (CBS) is a key coenzyme in GSH synthesis, and its deficiency is related to a variety of clinical diseases. However, whether CBS is involved in the pathogenesis of acute pancreatitis remains unclear. First, we found that CBS was downregulated in both in vivo and in vitro AP models. The pancreatic damage and acinar cell necrosis related to CBS deficiency were significantly improved by VB 12, which stimulated clearance of reactive oxygen species (ROS) by conserving GSH. Furthermore, EX-527 (a specific inhibitor of SIRT1) exposure counteracted the protective effect of VB 12 by promoting oxidative stress and aggravating mitochondrial damage without influencing CBS, indicating that vitamin B12 regulates SIRT1 to improve pancreatical damage by activating CBS. In conclusion, we found that VB 12 protected acute pancreatitis associated with oxidative stress via CBS/SIRT1 pathway.


2017 ◽  
Vol 6 (3) ◽  
pp. 353-360 ◽  
Author(s):  
Xueji Li ◽  
Liting Zhou ◽  
Yiping Ni ◽  
Aiqing Wang ◽  
Mingjiang Hu ◽  
...  

The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants.


2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.


2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.


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