Abstract

Herbal medicines played a major role in the treatment of hepatic disorders, and a number of medicinal plants and their compounds were widely used for the treatment of these disorders, and oxidant stress injury was one of the mechanism of liver injury. Antioxidant activity of Nelumbo nucifera leaves (NU) extracts was assayed by the methods of scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2'-azino-bis (3-ethylbenzo-thiazoline-6-sulfonicacid) (ABTS) radical and ferric reducing antioxidant power (FRAP) in vitro. By intraperitoneal injection carbon tetrachloride (CCl4) to establish acute liver injury model in mice, the levels of Glutamic-pyruvic transaminase (GPT), glutamic-oxaloacetic transaminase (GOT), superoxide dismutase (SOD) and the content of and maleicdialdehyde (MDA) were detected to evaluate hepatoprotective effect of NU using corresponding test kit. EtOAC (NUEA) and n-BuOH extracts (NUBU) of N. nucifera leaves had good scavenging DPPH and ABTS radical activity and ferric reducing antioxidant power in vitro. DPPH radical scavenging activity and ferric reducing antioxidant power of NUEA (IC50= 6.68±0.29 µg/mL, RACT50=1749.82±67.03 µmol/g) and NUBU (IC50= 4.61±0.01 µg/mL, RACT50=1995.27±135.71 µmol/g ) were higher than that of BHT (IC50=8.76±0.20 µg/mL, RACT50=1581.68±97.41 µmol/g) and Dangfeiliganning (IC50=28.06±0.17 µg/mL, RACT50=1028.55±3.28 µmol/g). ABTS radical scavenging activity of NUEA (IC50= 5.32±0.12 µg/mL) and NUBU (IC50= 8.16±0.27 µg/mL) were higher than that of Dangfeiliganning (IC50= 9.76±0.16 µg/mL). Thus, hepatoprotective effect of NUEA and NUBU was evaluated on CCl4-induced acute liver injury mice. The results showed that the levels of GOT and GPT in each treatment group significantly decreased (p<0.001 and p<0.01, p<0.05, respectively) except for the group of NUEA (130.8 mg/kg) (p>0.05). The contents of malondialdehyde (MDA) in liver in groups of NUEA (523 mg/kg), NUBU (840.5 and 420.5 mg/kg, repectively) had significant decrease (p<0.001 and p<0.05, respectively), and the level of SOD in liver for each treatment group could significantly decrease (p<0.001, p<0.05, respectively). NUEA and NUBU had significantly hepatoprotective effect for Calcium tetrachloride CCl4-induced liver injury, which might be attributable to its antioxidant activity.

Highlights

  • Liver injury can be induced by various factors, such as CCl4, ethanol and acetaminophen, which are metabolized by Cytochrome P450 2E1 (CYP2E1) to generate unstable free radicals and reactive oxygen species (ROS), these free radicals and ROS can induce liver cell apoptosis and necrosis (Sun et al, 2001; Kuzu et al, 2007), and up-regulation of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) in necrotic hepatocytes that accelerate the progression of liver cell injury

  • Treated group compared to CCL4-induced acute liver injury: *P

  • NUEA and NUBU could significantly decrease the levels of Glutamic-pyruvic transaminase (GPT) and glutamic-oxaloacetic transaminase (GOT) in serum, the content of MDA in liver homogenate solution and increase the level of superoxide dismutase (SOD) in liver homogenate solution in CCl4-induced liver injury mice model in vivo, which indicated that NUEA and NUBU had hepatoprotective effects against oxidant injury

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Summary

Introduction

Liver injury can be induced by various factors, such as CCl4, ethanol and acetaminophen, which are metabolized by Cytochrome P450 2E1 (CYP2E1) to generate unstable free radicals and reactive oxygen species (ROS), these free radicals and ROS can induce liver cell apoptosis and necrosis (Sun et al, 2001; Kuzu et al, 2007), and up-regulation of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) in necrotic hepatocytes that accelerate the progression of liver cell injury.Carbon tetrachloride (CCl4) is one of the oldest and most widely used toxins for experimental induction of liver injury in laboratory animals. The mechanism of CCl4-induced liver injury is accepted widely, CCl4 is metabolized to a highly reactive trichloromethyl free radical (CCl3-) and chlorine free radical (Cl-) by cytochrome P450 in liver microsome. Herbal medicines played a major role in the treatment of hepatic disorders, and a number of medicinal plants and their compounds were widely used for the treatment of these disorders, and oxidant stress injury was one of the mechanism of liver injury. Results: EtOAC (NUEA) and n-BuOH extracts (NUBU) of N. nucifera leaves had good scavenging DPPH and ABTS radical activity and ferric reducing antioxidant power in vitro. Conclusion: NUEA and NUBU had significantly hepatoprotective effect for Calcium tetrachloride CCl4-induced liver injury, which might be attributable to its antioxidant activity

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