scholarly journals Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

2015 ◽  
Vol 31 (2) ◽  
pp. 171-184 ◽  
Author(s):  
Krishnan Gokuladhas ◽  
Subramaniyan Jayakumar ◽  
Balan Rajan ◽  
Ramasamy Elamaran ◽  
Chengalvarayan Subramani Pramila ◽  
...  
Author(s):  
Nirmala Subramaniam ◽  
Pugazhendhi Kannan ◽  
Jagan Sundaram ◽  
Ashok Mari ◽  
Sathesh K. Velli ◽  
...  

Background: To evaluate the chemopreventive potential of boldine against diethylnitrosamine (DEN) induced hepatocellular carcinoma (HCC) in wistar albino rats. Objective: Boldine is an alkaloid isolated from Peumus boldus. The primary active constituents of boldine exhibited several potential medicinal properties. The present study was evaluated to explore the chemopreventive agent of boldine on anti-proliferative efficacy against diethylnitrosamine (DEN) induced hepatocellular carcinoma (HCC) in wistar albino rats. Methods: The effect of boldine on cellular proliferative markers, i.e., PCNA and Ki67 on hepatocellular carcinoma rats was determined by immuno expression study. Liver marker enzymes, tumor biomarker, oxidative stress markers, anti-oxidant status and xenobiotic phase I and II enzymes in HCC rats were analyzed. Moreover, cell cycle proteins, i.e., p21Cip1/Kip1, p27 Cip1/Kip1, Cyclin D1, CDK 4, Cyclin E1, and CDK 2 were investigated using immuno expression analysis. Results: Treatment of boldine protected the liver against reactive oxygen species such as hydrogen peroxide, superoxide, protein carbonyl and lipid peroxide during hepatocarcinogenesis by boosted antioxidants-superoxide dismutase (SOD), catalase (CAT). Boldine caused substantial enhanced detoxification process by moderating phase I and II xenobiotic metabolizing enzymes. In addition, the study was found that boldine significantly inhibited the cellular proliferative markers like PCNA and Ki67 and regulated the specific cell cycle associated proteins by up-regulated expression of p21Cip1/Kip1 and p27 Cip1/Kip1 and down-regulated expression of Cyclin D1, CDK 4, Cyclin E1, and CDK 2. Conclusion: Our data manifests the anti-proliferative effect of boldine, which negatively modulates cellular proliferation and regulates cell cycle by protecting the cell from reactive oxygen species (ROS), suggesting that boldine establish it as a chemopreventive agent in diethylnitrosamine-induced hepatocarcinogenesis in rats.


2007 ◽  
Vol 37 (s2 Fourth JSH S) ◽  
pp. S303-S307 ◽  
Author(s):  
Akihiro Tamori ◽  
Daiki Habu ◽  
Susumu Shiomi ◽  
Shoji Kubo ◽  
Shuhei Nishiguchi

2014 ◽  
Vol 38 (3) ◽  
pp. 774-782 ◽  
Author(s):  
Merve Bacanlı ◽  
Sevtap Aydın ◽  
Gökçe Taner ◽  
Hatice Gül Göktaş ◽  
Tolga Şahin ◽  
...  

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.


Hepatology ◽  
2014 ◽  
Vol 60 (3) ◽  
pp. 1110-1111 ◽  
Author(s):  
Emeric Limagne ◽  
Vanessa Cottet ◽  
Alexia Karen Cotte ◽  
Samia Hamza ◽  
Patrick Hillon ◽  
...  

2020 ◽  
Vol 113 ◽  
pp. 104622 ◽  
Author(s):  
Shahenda Mahgoub ◽  
Anas O. Sallam ◽  
Hazem K.A. Sarhan ◽  
Amal A.A. Ammar ◽  
Sameh H. Soror

Author(s):  
Saiprasanna Behera ◽  
S M Babu ◽  
Y Roja Ramani ◽  
Prasanta Kumar Choudhury ◽  
Sudeep Kumar Patra

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