Role of Human wharton's jelly derived Mesenchymal Stem cells (WJ-MSCs) for rescue of D-Galactosamine induced acute liver injury in mice

• Published in: Journal of clinical and experimental hepatology 2017-09, Vol.7 (3), p.205-214
• Main Authors: Raghu, Ramanathan, Secunda, Rupert, Sakthivel, Selvaraj, Jeswanth, Satyanesan, Vennila, Rosy, Surendran, Rajagopal
• Format: Article
• Language: English
• Subjects: cytogenetics; d-galactosamine; Endocrinology & Metabolism; Gastroenterology and Hepatology; hepatotoxicity; Original; oxidative stress; WJ-MSCs
• ISSN: 0973-6883; 2213-3453
• DOI: 10.1016/j.jceh.2017.03.010

Abstract Objective Mesenchymal stem cells (MSCs) are multipotent precursor cells having self-renewal ability making them a candidate for use in regenerative medicine. Acute liver injury results in sudden loss of hepatic function leading to organ failure. Liver Transplantation is often required to salvage patients with acute liver failure. Due to shortage of organs, identification of alternate method is the need of the hour. In view of this, an attempt has been made to check the regenerative ability of WJ-MSCs (wharton's jelly derived mesenchymal stem cell) in mice models for acute liver injury. Methods Swiss albino mice weighing 25 ± 5 g were used in this study. The control mice (Group I), was given saline. Group II mice received D-Galactosamine (D-GalN- 800 mg mg/kg.; i.p). Group III mice similar with Group II, received WJ-MSCs (5 × 105 cells/0.5 ml DMEM) through tail vein, 24 h after D-GalN administration and Group IV mice received MSC alone. Results Parameters, indicative of hepatotoxicity and oxidative stress were analyzed. A two-fold elevation in the marker enzymes of liver toxicity such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (SAP), & total serum bilirubin (TBIL) confirms hepatocellular injury, while a greater than four-fold increase in malondialdehyde (MDA) formation, along with around 40% fall in superoxide-dis-mutase (SOD) activity was indicative of oxidative stress and loss of hepatocellular membrane integrity induced by D-GalN. The above biochemical and pathological changes were significantly restored in mice that received WJ-MSCs indicating hepatoprotective and probable regenerative property. Conclusion The present study showed that WJ-MSC treatment is able to rescue/ameliorate the hepatotoxicity induced by D-GalN in mice.