Abstract
The present study was conducted to investigate the use of stearic acid-grafted carboxymethyl chitosan(SA-CMC) as a downregulator for trans- forming growth factor-β (TGF- β) and vascular endothelial growth factor (VEGF) in Ehrlich ascites carcinoma (EAC)-bearing mice. The antitumor effect of stearic acid-grafted carboxymethyl chitosan was assessed by the estimation of TGF- β and VEGF in serum in addition to the estimation of tumor volume, median survival time (MST), percentage of increase in life span (ILS%) as well as the contents of total lipid, DNA and RNA in liver tissues. Hematological profiles (hemoglobin, red blood cells, and platelets) were also assessed. In addition, liver function tests and the redox status were estimated. TGF- β, VEGF, DNA, RNA, and malondialdehyde (MDA) levels, in addition to serum alanine transaminase (ALT) and gamma glutamyl transferase (GGT) activities as well as total white blood cells counts and tumor volume were all highly significantly increased (P < 0.001) in untreated EAC-bearing mice compared to controls. However, hematological profiles, total lipid in liver tissues and serum albumin were highly decreased in EAC-bearing mice compared to controls. All these parameters were restored to the normal levels in SA-CMC treated EAC-bearing mice com- pared to the untreated EAC-bearing mice. It is thus concluded that stearic acid-grafted carboxymethyl chitosan has a remarkable antitumor activity against EAC in Swiss albino mice through downregulation of TGF-β and VEGF.
Highlights
Many studies have demonstrated the role of reactive oxygen species (ROS) in tumor development [1]
The scavenging ability is related to the number of active hydroxyl groups in the molecule [8]
Carboxymethyl chitosan was prepared by the method of Liu et al [21]. 10 g of chitosan (8.4 × 104, the degree of deacetylation 85%) purchased from Sigma Aldrich, USA, 13.5 g sodium hydroxide and 100 ml of isopropanol mixed in a 500 ml flask at 50 ̊C for 1 h and 15 g of monochloroacetic acid dissolved in 20 ml isopropanol were added into the reaction mixture dropwise for 30 min
Summary
Many studies have demonstrated the role of reactive oxygen species (ROS) in tumor development [1]. ROS can be produced from endogenous sources, such as from mitochondria, peroxisomes, and inflammatory cell activation [2]; and exogenous sources, including environmental agents, pharmaceuticals, and industrial chemicals. The free radicals which include both reactive oxygen species such as, superoxide (O2−), hydroxyl (OH−), hydroperoxyl (HOO−), peroxyl (ROO−) and alkoxyl (RO−) radicals and nitrogen (RNS) species are highly active and generally unstable [3]. The uncontrolled oxidative stresses due to excessive production of active oxygen or imbalance in body’s redox potential have been implicated in diverse processes in various cancers, and generally the increase of ROS in cancer cells is known to play an important role in the initiation and progression of cancer [5]. Superoxide dismutases (SODs) are metalloenzymes that catalyze the dismutation of superoxide anions into molecular oxygen and hydrogen peroxide; OPEN ACCESS
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