scholarly journals Effect of aqueous extract of Capparis spinosa on biochemical and histological changes in paracetamol–induced liver damage in rats

2012 ◽  
Vol 26 (1) ◽  
pp. 1-10
Author(s):  
H. I. A. Al-khan ◽  
R. J. M. Alnuaimy
Author(s):  
Sumra Komal

Introduction: Hepatic diseases remain the leading cause of death worldwide. Despite overall advancements in health care, mortality due to hepatic diseases is constantly growing. More than 2 million people globally are estimated to die each year from liver diseases, and current treatment offers little for its management. Thus, it is essential to find more effective and less toxic pharmaceutical alternatives for the treatment of liver diseases. Aims & Objectives: Tamarix dioica, a shrub broadly used in herbal medicine for the treatment and prevention of various diseases. The current study was designed to analyze the hepatoprotective effect of T. dioica in BALB?cmice against CCl4-induced acute liver damage. Place and duration of study: The study was conducted in NIH, Islamabad, Pakistan, for six months in 2016-2017. Material & Methods: For in vivo evaluation, the animals (n= 42) were randomly divided into seven groups (n=6), three control (i.e. Group, I or normal control, group II or induction control received 0.9% normal saline orally, and Group III or positive control received silymarin 100 mg/kg per oral), and four treatment groups (i.e. IV, V,VI and VII were treated with oral T.dioica 200 mg/kg/day, 300mg/kg/day methanol extract, 200mg/kg/day and 300mg/kg/day of aqueous extracts respectively for six days, followed by intraperitoneal administration of CCl4 on the seventh day. The blood samples were collected for analysis of LFTs, and hepatic tissue was taken for histological analysis. Data was analyzed using SPSS version 16, one-way ANOVA with Duncan’s Multiple Range Test (DMRT). Results: CCl4 induction in Group 2 resulted in severe hepatic derangement manifested as highly elevated mean LFTs (ALT 7245.56, AST 3292.11, ALP 340.09 U/L, bilirubin 4.64 mg/dl) as compared to healthy controls (ALT 38.97, AST 50.20, ALP 57.17 U/L, bilirubin 1.25 mg/dl: (Group 1) levels p<0.001. Pretreatment with different extracts of T.dioica for 6 days before CCl4 administration produced varying degrees of hepatoprotection. 300mg/kg aqueous extract T.dioica (Group7) prevented damage with maximal hepatoprotection, reduced LFTs (ALT: 339.95 , AST: 242.90 , ALP: 116.86 U/L, bilirubin: 1.38 mg/dl) and normalized liver histology as compared to Group 2 and standard drug silymarin 100mg/kg, (ALT: 6483.23, AST: 2567.69, ALP: 272.19 U/L, bilirubin: 2.84 mg/dl: Group 3) p<0.001. Lesser hepatoprotection was provided by T.dioica aqueous extract 200mg/kg (ALT: 439.93, AST: 367.87, ALP: 180.62 U/L bilirubin: 1.53 mg/dl: Group VI) and least by 300mg/kg & 200mg/kg methanolic extracts Groups V & IV (ALT: 6338.06, 6443.91, AST: 2800.81, 3012.34, ALP: 242, 248 U/L & bilirubin: 2.82 & 3.62 mg/dl) respectively. Further, no drug-induced toxicity symptoms were observed 24 hours after administration of the high dose oral T. dioica 2000 mg/kg/body weight aqueous and methanolic extracts were administered. Conclusion: Pretreatment with T. dioica extracts especially 300mg/kg aqueous extract reduced acute CCl4-mediated liver damage, ameliorated histopathological as well as biochemical parameters and was free of toxicity in 2000mg/kg /body weight dose in the mice experimental model. T. dioica has potential in hepatoprotective drug research.


2015 ◽  
Vol 15 (1) ◽  
pp. 2 ◽  
Author(s):  
SI Omoruyi ◽  
AB Enogieru ◽  
OI Momodu ◽  
BA Ayinde ◽  
BD Grillo

Author(s):  
Rojini Athokpam ◽  
Meenakshi Bawari ◽  
Manabendra Dutta Choudhury

  Objective: To evaluate the hepatoprotective activity of aqueous extract of Oxalis debilis Kunth in carbon tetrachloride (CCl4)-induced hepatotoxicity in Swiss albino mice.Methods: Hepatotoxicity was induced by CCl4 30% in olive oil (1 ml/kg intraperitoneally). Mice were treated with aqueous extract of O. debilis at doses of 250 and 500 mg/kg body weight orally for 14 days. There were two groups, pre-treatment (once daily for 14 days before CCl4 intoxication) and post-treatment (2, 6, 24, and 48 hrs after CCl4 intoxication). The observed effects were compared with a known hepatoprotective agent, silymarin.Results: Pre-treatment and post-treatment groups of aqueous extract of O. debilis significantly reduced elevated serum levels of serum transaminases, alkaline phosphatase, and bilirubin and increased the level of total protein as compared to CCl4-treated group. The histopathological study also confirms the hepatoprotection. Preliminary qualitative phytochemical analysis of the plant revealed the presence of phenolic compounds, tannins, flavonoids, and saponins.Conclusion: The results of this study suggest that O. debilis can be used as safe, cheap, and alternative preventive and protective drugs against liver injury. The protective effect observed could be attributed to the presence of various phytochemicals which are responsible for the restoration of liver damage.


Author(s):  
Medhat Mostafa Abozid ◽  
Hoda Ea Farid

 Objective: The current study was designed to estimate the potential protective role of the aqueous extract of rosemary (AER) (Rosmarinus officinalis) against trichloroacetic acid (TCA)-created hepatotoxicity in male albino rats.Methods: Forty male albino rats were separated into four groups of ten: Group I served as control; Group II was given AER (200 mg/kg/day) by gavage; Group III received TCA at the dose 50 mg/kg/day, and Group V was treated with AER (200 mg/kg/day) and received TCA (50 mg/kg/day). The experiment was carried out for 2 months.Results: The toxicity of TCA for rats was revealed by an elevation in liver marker enzymes activities (gamma-glutamyl transferase [GGT], alkaline phosphatase [ALP], aspartate transaminase [AST], alanine aminotransferase [ALT]) and conjugated bilirubin (CB) level, and a decrease in albumin and total protein (TP) levels. The TCA administration also caused a significant increase in the activities of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), and also malondialdehyde (MDA) level in liver tissues. These biochemical effects were accompanied by histological indicators of liver damage. Treatment with ARE recovered the liver damage instigated by TCA, as showed by perfection of liver enzyme markers (GGT, ALT, AST, ALP), CB, TP and albumin; as well as antioxidant parameters (CAT, SOD, GPx) and lipid peroxidation (MDA) and amelioration of histopathology changes in the liver tissues.Conclusion: It could be concluded that AER supplementation for 2 months in TCA-induced toxicity in rats benefited hepatic antioxidant status and improved liver injury and damage in male albino rats exposed to TCA.


1974 ◽  
Vol 31 (8) ◽  
pp. 1397-1400 ◽  
Author(s):  
Y. Malevski ◽  
J. H. Wales ◽  
M. W. Montgomery

Histological changes in livers of rainbow trout (Salmo gairdneri) repeatedly fed diets containing cyclopropenoid fatty acids (CPFA) revealed that these fish were unable to develop resistance to liver damage caused by CPFA. One group of trout was fed 150 ppm CPFA in the basal diet for 49 days followed by the basal diet for the remainder of the experimental period. Another group of trout was fed 150 ppm CPFA for 49 days, basal diet for 65 days, and 150 ppm CPFA for 45 days. At this time this group was divided into two subgroups; one received basal diet for 15 days, the other for 30 days, after which both subgroups were placed on a diet containing 360 ppm CPFA for 36 days. Analysis of the livers for histological changes showed that the parenchymal cells underwent cyclic changes of injury and recovery each time the trout were fed CPFA. Complete recovery of parenchymal cells occurred after the fish were removed from the diets containing CPFA for 30 days. Bile duct and blood vessel hyperplasia was observed for as long as 7 mo after CPFA was eliminated from the trout diet.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 651-651
Author(s):  
Matteo Iannacone ◽  
Giovanni Sitia ◽  
Masanori Isogawa ◽  
Patrizia Marchese ◽  
Maria G. Castro ◽  
...  

Abstract We used hepatitis B virus (HBV) transgenic mice as recipients of cytotoxic T cells (CTLs) specific for the immunodominant Env28–39 epitope (Env28) of HbsAg, and C57BL/6J mice acutely infected with a recombinant replication-deficient adenovirus expressing lacZ (RAd35) to show that platelets accumulate in necroinflammatory foci of the liver during the course of a disease similar to acute hepatitis in humans. Liver disease was monitored by quantifying the activity of serum alanine aminotransferase (sALT), a hepatocellular enzyme that is released into the circulation by necrotic hepatocytes, and by evaluating histological changes at the time of autopsy. Livers from mice sacrificed 2 days after CTL transfer were stained with a mixture of rat monoclonal antibodies (α-PLT) against mouse glycoprotein (GP) Ibα, a receptor exclusively expressed on platelets and megakaryocytes. Livers from mice injected with saline (0.9% NaCl) alone served as controls. Platelets were detectable only inside vessels and hepatic sinusoids in saline-injected controls, while they accumulated alongside apoptotic hepatocytes and inflammatory cells within necroinflammatory foci of the liver in CTL-injected or RAd35-infected animals. The injection of α-PLT caused a &gt;97.5% decrease in the number of circulating platelets (less than 2x104 platelets/μl of blood) within 30 min, and similar low counts were maintained for up to 6 days. Mice that received either saline or an irrelevant antibody (α-Irr) exhibited stable platelet counts (8–10 x 105 platelets/μl of blood). Previous platelet depletion in CTL-injected or RAd35-infected animals reduced the intrahepatic accumulation of virus-specific CTLs and the resulting liver damage, as evidenced by an 80% reduction in sALT activity (from 1600 to 300 U/L) and a reduction the size of necroinflammatory foci (from 6724 μm2 to 1245 μm2) as compared to mice that received α-Irr. Infusion of washed mouse platelets expressing human GP Ibα (thus, insensitive to the depleting effect of α-Plt) within hours after CTL transfer or RAd35 infection restored CTL accumulation and liver disease severity, but not when the infused platelets were pretreated with the activation inhibitor, prostaglandin E1. Accordingly, platelet activation was required to promote CTL/platelet interactions under flow conditions in vitro. Fibrin deposition was abundant within hepatic necroinflammatory foci of CTL-injected or RAd35-infected animals, and markedly decreased in animals that were previously made thrombocytopenic. The platelet-dependent intrahepatic deposition of fibrin could be selectively prevented by anticoagulant treatment of the mice, which had no effect on the platelet count, but this did not ameliorate liver injury. Our findings indicate that activated platelets contribute to CTL-induced liver immunopathology by facilitating the accumulation of CTLs at the site of inflammation, independently of procoagulant function.


1995 ◽  
Vol 23 (01) ◽  
pp. 65-69 ◽  
Author(s):  
Chun-Ching Lin ◽  
Wei-Chih Lin ◽  
Shaw-Rong Yang ◽  
Den-En Shieh

Solanum alatum aqueous extract was investigated on carrageenin-induced edema and on CCl 4-induced liver injury. The extract (100 or 200 mg/kg body weight) exhibited both anti-inflammatory and hepatoprotective activities. The effects were more prominent at the dose of 200 mg/kg. Histological changes such as necrosis, fatty changes, ballooning degeneration, and inflammatory infiltration of lymphocytes and Kupffer cells around the central veins were concurrently improved by treatment with the S. alatum aqueous extract.


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