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1.
The rate of rise of body temperature and the survival time on exposure to a temperature of 40°C was recorded in normal Wistar rats and those given ip injection of 1 ml/kg BW of CCl4 24 h earlier with and without administration of (a) garlic oil (0.006 ml in arachis oil) 3 days earlier, (b) Dl--tocopherol (450 mg/kg BW) 48 h before CCl4 (c) glucose (300 mg in 2 ml saline) 30 min before exposure to heat stress. Significant protection against the reduction in heat tolerance by CCl4 was provided by glucose and garlic but not by vitamin E. The reduction in heat tolerance by CCl4 was attributed to the hypoglycemia caused by it, followed by breakdown of the thermoregulatory centres in the hypothalamus. The protective effect of glucose was attributed to the restoration of blood glucose levels and that of the garlic oil to its protective effect on hepatocytes against CCl4 toxicity. 相似文献
2.
Sabry M Shaarawy Amany A Tohamy Saad M. Elgendy Zakaria Y Abd Elmageed Abeer Bahnasy Maha S Mohamed Emad Kandil Khalid Matrougui 《International journal of biological sciences》2009,5(6):549-557
Background — The present study was conducted to investigate the chemopreventive effects of garlic extract and silymarin on N-nitrosodiethylamine (NDEA) and carbon tetrachloride (CCl4)-induced hepatotoxicity in male albino rats. Methods and Results — Animals were pretreated with garlic, silymarin or both for one week prior to the injection of NDEA. Then animals received a single injection of NDEA followed by weekly subcutaneous injections of CCl4 for 6 weeks. Oral administration was then continued along with the injection of CCl4 for the duration of the experiment. Serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), hepatic lipid peroxidation (LPO), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-S-transferase (GST) and glutathione reductase (GSR) were measured. Injection of NDEA induced a significant elevation in serum AST, ALT and ALP. In the liver, NDEA increased oxidative stress through the increase in LPO and decrease in SOD, and GSH-dependent enzymes. Although administration of garlic or silymarin significantly reduced the liver toxicity, combined administration was more effective in preventing the development of hepatotoxicity. Conclusion — These novel findings suggest that silymarin and garlic have a synergistic effect, and could be used as hepatoprotective agents against hepatotoxicity. 相似文献
3.
4.
The present study aimed at detecting DNA damage and fragmentation as well as histone acetylation depending on oxidative stress caused by CCl4 intoxication. Also, the protective role of N-acetyl cysteine, a precursor for GSH, in DNA damage is investigated. Sixty rats were used in this study. In order to induce liver toxicity, CCl4 in was dissolved in olive oil (1/1) and injected intraperitoneally as a single dose (2 ml/kg). N-acetyl cysteine application (intraperitoneal, 50 mg/kg/day) was started 3 days prior to CCl4 injection and continued during the experimental period. Control groups were given olive oil and N-acetyl cysteine. After 6 and 72 h of CCl4 injection, blood and liver tissue were taken under ether anesthesia. Nuclear extracts were prepared from liver. Changes in serum AST and ALT activities as well as MDA, TAS, and TOS levels showed that CCl4 caused lipid peroxidation and liver damage. However, lipid peroxidation and liver damage were reduced in the N-acetyl cysteine group. Increased levels in 8-hydroxy-2-deoxy guanosine and histone acetyltransferase activities, decreased histone deacetylase activities, and DNA breakage detected in nuclear extracts showed that CCl4 intoxication induces oxidative stress and apoptosis in rat liver. The results of the present study indicate that N-acetyl cysteine has a protective effect on CCl4-induced DNA damage. 相似文献
5.
The ability of Cichorium intybus root extract (chicory extract) to protect against carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity was evaluated in male rats. The rats were divided into four groups according to treatment: saline (control); chicory extract (100 mg/kg body weight daily, given orally for 2 weeks); CCl4 (1 ml/kg body weight by intraperitoneal injection for 2 consecutive days only); or chicory extract (100 mg/kg body weight daily for 2 weeks) + CCl4 injection on days 16 and 17. The levels of hepatic lipid peroxidation, antioxidants, and molecular biomarkers were estimated twenty-four hours after the last CCl4 injection. Pretreatment with chicory extract significantly reduced CCl4-induced elevation of malondialdehyde levels and nearly normalized levels of glutathione and activity of glutathione S-transferase, glutathione peroxidase (GPx), glutathione reductase, catalase (CAT), paraoxonase-1 (PON1), and arylesterase in the liver. Chicory extract also attenuated CCl4-induced downregulation of hepatic mRNA expression levels of GPx1, CAT and PON1 genes. Results of DNA fragmentation support the ability of chicory extract to ameliorate CCl4-induced liver toxicity. Taken together, our results demonstrate that chicory extract is rich in natural antioxidants and able to attenuate CCl4-induced hepatocellular injury, likely by scavenging reactive free radicals, boosting the endogenous antioxidant defense system, and overexpressing genes encoding antioxidant enzymes. 相似文献
6.
The protective effect of taurine pretreatment on carbon tetrachloride-induced hepatic damage--a light and electron microscopic study 总被引:1,自引:0,他引:1
Summary. The results regarding taurine pretreatment on CCl4-induced hepatic injury are controversial. To assess the therapeutic efficacy of taurine on rat liver injury, hepatic malondialdehyde,
glutathione, and hydroxyproline levels together with morphologic alterations in the liver following CCl4 administration were investigated. The rats were divided into three groups. Taurine-treated animals received 15 ml/kg/day
of a 5% taurine solution by a gastric tube for 5 days before administering CCl4 (2 ml/kg, intraperitoneally, in a single dose). CCl4-treated rats received the same amount of saline solution. Control animals received no treatment. The increase of hepatic
malondialdehyde formation in the CCl4-treated group was partially prevented by taurine pretreatment, but taurine had no significant effect on the glutathione and
hydroxyproline content in the CCl4-treated rats. Taurine pretreatment induced a marked beneficial effect regarding the prevention of hepatocellular necrosis
and atrophy as demonstrated morphologically. In conclusion, these results suggest that taurine pretreatment might not significantly
change the biochemical parameters, but prevents the morphologic damage caused by CCl4 in the early stages.
Received March 17, 2001 Accepted July 18, 2001 相似文献
7.
Rui Jia Liping Cao Jinliang Du Pao Xu Galina Jeney Guojun Yin 《In vitro cellular & developmental biology. Animal》2013,49(3):155-161
Silymarin, a mixture of bioactive flavonolignans from the milk thistle (Silybum marianum), is traditionally used in herbal medicine to defend against various hepatotoxic agents. The aim of the present study was to evaluate the protective effect of silymarin against carbon tetrachloride (CCl4)-induced liver injury in fish. Common carp, with an average initial weight of 17.0?±?1.1 g, were fed diet containing four doses of silymarin (0, 0.1, 0.5, and 1 g/kg diet) for 60 d. Fish were then given an intraperitoneal injection of CCl4 (30% in arachis oil) at a dose of 0.5 ml/kg body weight. At 72 h after CCl4 injection, blood and liver samples were collected for the analyses of serum biochemical parameters, liver index, peroxidation product, glutathione, and antioxidant enzyme activities. The results showed that administration of silymarin at 0.5 and 1 g/kg diet for 60 d prior to CCl4 intoxication significantly reduced the elevated activities of glutamate pyruvate transaminase, glutamate oxalate transaminase, lactate dehydrogenase (LDH), and increased the reduced levels of total protein and albumin in the serum. The reduced levels of liver index, superoxide dismutase, glutathione peroxidase, catalase, glutathione, and total antioxidant capacity were markedly increased, and malondialdehyde formation was significantly restrained in the liver. However, these parameters, except LDH, were not significantly changed in fish fed with silymarin at 0.1 g/kg diet. Based on the results, it can be concluded that silymarin has protective effect against CCl4-induced hepatotoxicity in fish. It is suggested that silymarin may be used as a hepatoprotective agent to prevent liver diseases in fish. 相似文献
8.
Ying Yao Liping Wang Peipei Jin Na Li Yan Meng Changli Wang Mengda Xu Yan Zhang Jinjun Bian Xiaoming Deng 《Journal of molecular histology》2017,48(4):301-310
The inflammatory response plays an important role in carbon tetrachloride (CCl4)-induced acute liver injury and methane has been shown to exert beneficial effects on inflammation-associated diseases. Thus, we investigated the potential protective effects of methane-rich saline (MS) on CCl4-induced acute liver injury and explored the underlying mechanism. A CCl4-induced acute liver injury model was established by injection of CCl4 (0.6 ml/kg, ip) in mice followed by treatment with MS (16 ml/kg, ip), 24 h later. All groups of mice were sacrificed and blood and liver tissues were collected. Serum aminotransferase, necrotic areas, and inflammatory cell infiltration in liver slices were enhanced after CCl4 treatment but decreased with MS treatment. IL-6, TNF-α, IL-1β, IFN-γ, ICAM-1, CXCL1, MPO, NF-κB p65, ERK, JNK, and MAPK P38, expression in serum or liver homogenate were greater after CCl4 treatment but comparatively less after MS treatment. Only IL-10 increased after MS treatment. Anti-IL10 blockade (1.5 mg/kg) restored MS-mediated attenuated phosphorylation of NF-?bB/MAPK and the protective effect of MS was abolished for all indices examined. The PI3K inhibitor, wortmannin had the same effects on MS as anti-IL-10 antibody. MS also induced phosphorylation of GSK-3β and AKT in CCl4-treated mice. After pre-treatment with wortmannin (0.7 mg/kg), phosphorylation of GSK-3β and AKT proteins were reduced compared to its solvent control group-DMSO-treated animals. Thus, the data provide evidence that MS may activate the PI3K–AKT–GSK-3β pathway to induce IL-10 expression and produce anti-inflammatory effects via the NF-κB and MAPK pathways. The findings provide a new pharmacological strategy for management of inflammatory response after acute liver injury. 相似文献
9.
Mervi T. Hyvönen Riitta Sinervirta Nikolay Grigorenko Alex R. Khomutov Jouko Vepsäläinen Tuomo A. Keinänen Leena Alhonen 《Amino acids》2010,38(2):575-581
The role of polyamines in carbon tetrachloride (CCl4)-induced organ injury was studied in syngenic rats and transgenic rats with activated polyamine catabolism. In syngenic rats,
administration of CCl4 resulted in the induction of hepatic spermidine/spermine N
1-acetyltransferase (SSAT), accumulation of putrescine, reduction in spermine level and appearance of moderate hepatic injury
within 24 h. Upon treatment with CCl4, transgenic rats overexpressing SSAT displayed induction of both hepatic and pancreatic SSAT, with subsequent accumulation
of putrescine and decrease of both spermidine and spermine pools. Administration of CCl4 in SSAT transgenic rats induced not only massive hepatic injury, but also severe acute necrotizing pancreatitis. Pretreatment
of the animals with catabolically stable functional polyamine mimetic, α-methylspermidine (MeSpd) prevented pancreatic and
hepatic injury in SSAT rats and markedly reduced liver damage in syngenic animals. As assessed by immunostaining of proliferating
cell nuclear antigen, MeSpd increased the amount of regenerating hepatocytes in both genotypes. These results show that CCl4 induces hepatic and pancreatic polyamine catabolism, and the extent of organ damage correlates with the degree of polyamine
depletion. Furthermore, MeSpd protects against CCl4-induced hepatic and pancreatic damage and promotes tissue regeneration. 相似文献
10.
Hasan Yousefi-Manesh Samira Shirooie Alireza Partoazar Vahid Nikoui Mohammad Reza Abdollahzadeh Estakhri Azam Bakhtiarian 《Journal of cellular biochemistry》2019,120(7):11853-11858
It has been proposed carbon tetrachloride (CCl4) intoxication due to the production of free radicals and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) overload results hepatotoxicity. Phosphatidylserine (PS) has shown antioxidant activity in numerous studies. Therefore, this study was aimed to investigate the effects of PS liposomes treatment against the CCl4-induced hepatotoxicity in a rat model. Male Wistar rats were treated with PS (10 mg/kg, oral) or phosphatidylcholine liposomes (PC) (10 mg/kg, oral) for 3 days before CCl4 (2 ml/kg; ip once on the third day) injection. The serum level of ALT, AST, and ALP were measured. Also, antioxidant assays were performed. Administration of PS with CCl4 significantly inhibited alterations in the serum levels of AST, ALP (**P < 0.01), and ALT (***P < 0.001) compared with control group. Furthermore, measurement of malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels indicated that PS significantly reduced reactive oxygen species. The results of the present study showed the hepatoprotective effects of PS against CCl4-induced hepatotoxicity in rats. 相似文献
11.
Marzieh Ghasemi Mahnaz Azarnia Mansoor Jamali Ghadireh Mirabolghasemi Shahram Nazarian Mohammad Mehdi Naghizadeh Majid Rajabi Yaser Tahamtani 《Tissue & cell》2014
Inflammation and oxidation are two important factors in the pathogenesis of liver. Ephedra pachyclada (EP) is a traditional medical herb that has anti-inflammatory and anti-oxidant activities. During this study, anti-oxidant activities of the EP extract was measured in vitro by 2,2′- diphenyl-1-picrylhydrazyl (DPPH) and β-Carotene bleaching assays. Then, we examined possible in vivo hepatoprotective effects of EP extract on mouse models of carbon tetrachloride (CCl4)-induced chronic and acute liver failure. To produce mouse models of chronic and acute liver injuries, male SW1 mice were interaperitoneally injected with 1 ml/kg body weight (bw) CCl4 biweekly for 42 days and a single dose of 2 ml/kg bw, respectively. In the experimental groups, mouse models were treated with low (140 mg/kg bw) and high (1400 mg/kg bw) doses of the EP extract. Olive oil and water treated mice were considered as controls during model derivation and EP extract treatment respectively. The results showed the antioxidant activity of EP extract and a significant reduction of all parameters of CCl4-induced liver injury such as relative liver weight, necrosis, fibrosis, inflammation, and serum aspartate transaminase (AST) and alanine aminotransferase (ALT) in mouse models of acute and chronic liver injury treated with EP extract. Therefore, EP induces its hepatoprotective effects probably by suppressing oxidative stress and inhibit inflammation in the liver and is able to protect the liver against CCl4-induced acute and chronic injuries. 相似文献
12.
Fall in rectal temperature (Tre) and survival time was determined on exposure to–20°C in adult normoglycemic and diabetic (streptozotocin treated) rats and 1 h following glucose feeding or insulin administration or both and on exposure to–10°C in young rats with and without glucose feeding. The susceptibility to frostbite was determined by exposure of the limbs to freezing mixture of–19°C or–23°C. The rate of fall of Tre was less and the survival time more in glucose and insulin plus glucose treated animals. On the other hand, the rate of fall of Tre was more and the survival time less, in dia betic and insulin-treated animals. The rectal temperature at which the animal died was the same in the control and the treated animals. The susceptibility to frost bite was more in insulin treated and diabetic animals and less in glucose-fed animals. Exposure to cold during the second h after glucose or glucose plus insulin injection did not alter the blood glucose from that obtained at room temperature. In insulin-treated animals the rate of rise of blood glucose during the second h was much higher at low temperature than at room temperature. The rise in blood glucose in diabetic animals was much higher than in normoglycemic animals exposed to cold. 相似文献
13.
Young Ji Choi Da Hye KimSang Jun Kim Ju KimSeung-Il Jeong Chang Ho ChungKang-Yeol Yu Seon-Young Kim 《Life sciences》2014
Aims
We studied that a potent antifibrotic effect of decursin on in vivo liver damage model and the mechanism in inhibiting which transforming growth factor (TGF)-β1-induced human hepatic stellate cells (HSCs) activation.Main methods
Liver injury was induced in vivo by intraperitoneal injection of carbon tetrachloride (CCl4) with or without decursin for 4 weeks in mice. Human hepatic stellate cell line, an immortalized human HSC line, was used in in vitro assay system. The effects of decursin on HSC activation were measured by analyzing the expression of α-smooth muscle actin (α-SMA) and collagen I in liver tissue and human HSCs.Key findings
Decursin treatment significantly reduced the ratio of liver/body weight, α-SMA activation, and type I collagen overexpression in CCl4 treated mice liver. The elevated serum levels, including ALT, AST, and ALP, were also decreased by decursin treatment. Treatment of decursin markedly proved the generation of reactive oxygen species, NAD(P)H oxidase (NOX) protein (1, 2, and 4) upregulation, NOX activity, and superoxide anion production in HSCs by TGF-β1. It also significantly reduced TGF-β1-induced Smad 2/3 phosphorylation, nuclear translocation of Smad 4, and association of Smad 2/3–Smad 4 complex. Consistent with in vitro results, decursin treatment effectively blocked the levels of NOX protein, and Smad 2/3 phosphorylation in injured mice liver.Significance
Decursin blocked CCl4-induced liver fibrosis and inhibited TGF-β1-mediated HSC activation in vitro. These data demonstrated that decursin exhibited hepatoprotective effects on experimental fibrosis, potentially by inhibiting the TGF-β1 induced NOX activation and Smad signaling. 相似文献14.
15.
Aim
The objective of this study was to examine whether MT plays a protective role against the damage in the liver by administering carbontetrachloride (CCl4) to rats.Main method
28 male Wistar albino (n = 28, 8 weeks old) rats have been used in the study. The rats were distributed into 4 groups according to their live weights. The groups were: (i) negative control (NC): normal water consuming group to which no CCl4 and milk thistle (MT) is administered; (ii) positive control (PC): normal water consuming group to which no CCl4 is administered but MT is administered; (iii) CCl4 group: normal water consuming and group to which CCl4 is administered (2 ml/kg live weight, ip); and (iv) CCl4 + MT group: CCl4 and MT administered group (2 ml/kg live weight, ip). Caspase-3, caspase-9, bax, and bcl-2 protein syntheses were examined via western blotting. MDA determination in liver tissue was made using spectrophotometer.Key findings
MDA amount has decreased in the CCl4 + MT group in comparison to CCl4 group whereas caspase-3 and caspase-9 has increased and bax and bcl-2 has decreased.Significance
These results show that MT protects the liver against oxidative damage. 相似文献16.
Kim B. Pælestik Nichlas R. Jespersen Rebekka V. Jensen Jacob Johnsen Hans Erik Bøtker Steen B. Kristiansen 《Cardiovascular diabetology》2017,16(1):148
Background
Hypoglycemia is associated with increased mortality rate in patients with diabetes. The underlying mechanisms may involve reduced myocardial tolerance to ischemia and reperfusion (IR) or reduced capacity for ischemic preconditioning (IPC). As IPC is associated with increased myocardial glucose uptake (MGU) during reperfusion, cardioprotection is linked to glucose metabolism possibly by O-linked β-N-acetylglucosamine (O-GlcNAc). We aimed to investigate the impact of hypoglycemia in hearts from animals with diabetes on myocardial IR tolerance, on the efficacy of IPC and whether modulations of MGU and O-GlcNAc levels are involved in the underlying mechanisms.Methods
In a Langendorff model using diabetic ZDF (fa/fa) and non-diabetic (fa/+) rats (n = 6–7 in each group) infarct size (IS) was evaluated after 40 min of global ischemia and 120 min reperfusion during hypoglycemia [(glucose) = 3 mmol/l] and normoglycemia [(glucose) = 11 mmol/l]. Myocardial glucose uptake and O-GlcNAc levels were evaluated during reperfusion. IPC was induced by 2 × 5 min of global ischemia prior to index ischemia.Results
IS increased in hearts from animals with (p < 0.01) and without (p < 0.01) diabetes during hypoglycemia compared to normoglycemia. IPC reduced IS during normoglycemia in both animals with (p < 0.01) and without (p < 0.01) diabetes. During hypoglycemia, however, IPC only reduced IS in hearts from animals with diabetes (p < 0.05). IPC increased MGU during reperfusion and O-GlcNAc levels in animals with diabetes during hypo- (MGU: p < 0.05, O-GlcNAc: p < 0.05) and normoglycemia (MGU: p < 0.01, O-GlcNAc: p < 0.05) and in animals without diabetes only during normoglycemia (MGU: p < 0.05, O-GlcNAc: p < 0.01).Conclusions
Hypoglycemia increases myocardial susceptibility to IR injury in hearts from animals with and without diabetes. In contrast to hearts from animals without diabetes, the hearts from animals with diabetes are amenable to cardioprotection during hypoglycemia. In parallel with IPC induced cardioprotection, MGU and O-GlcNAc levels increase suggesting that increased MGU and O-GlcNAc levels are involved in the mechanisms of IPC.17.
The Protective Roles of IL‐6 Trans‐Signaling Regulated by ADAM9 on the Liver in Carbon Tetrachloride‐Induced Liver Injury in Mice
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San‐Qiang Li Dong‐Mei Wang Sha Zhu Hong‐Ye Meng Hong‐Mei Han Hua‐Jie Lu 《Journal of biochemical and molecular toxicology》2015,29(7):340-348
Our study was undertaken to evaluate the important role that a disintegrin and metalloproteinase 9 (ADAM9) regulates IL‐6 trans‐signaling in carbon tetrachloride (CCl4)‐induced liver injury in mice. Mice were divided into four groups. Each group respectively received mineral oil injection, CCl4 injection, anti‐ADAM9 monoclonal antibody (mAb) pretreatment and CCl4 injection, anti‐ADAM9 mAb and recombinant mouse ADAM9 molecules pretreatment with CCl4 injection. Our results showed that anti‐ADAM9 mAb pretreatment significantly aggravated liver injury, inhibited IL‐6 trans‐signaling, which led to downregulation of proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), upregulation of Caspase3, cytochrome P450 2E1 (CYP2E1), and hepatocytes apoptosis at 24 h after CCl4 injection. Recombinant ADAM9 molecules pretreatment reversed the impact of anti‐ADAM9 mAb pretreatment in mice. In conclusion, our study suggested that ADAM9 could regulate the hepatocytes proliferation, apoptosis, angiogenesis, and CYP2E1 expression by activating IL‐6 trans‐signaling and play important protective roles during CCl4‐induced liver injury in mice. 相似文献
18.
Induction of CYP 2E1 by carbon tetrachloride (CCl4) is one of the central pathways by which CCl4 generates oxidative stress in hepatocytes. Experimental liver injury was induced in rats by CCl4 to determine toxicological actions on CYP 2E1 by microsomal drug metabolizing enzymes. In this report, ethanolic extract
of propolis at a dose of 200 mg/kg (po) was used after 24 h of toxicant administration to validate its protective potential.
Intraperitoneal injection of CCl4 (1.5 ml/kg) induced hepatotoxicity after 24 h of its administration that was associated with elevated malonyldialdehyde (index
of lipid peroxidation), lactate dehydrogenase and γ-glutamyl transpeptidase release (index of a cytotoxic effect). Hepatic
microsomal drug metabolizing enzymes of CYP 2E1 showed sharp depletion as assessed by estimating aniline hydroxylase and amidopyrine
N-demethylase activity after CCl4 exposure. Toxic effect of CCl4 was evident on CYP 2E1 activity by increased hexobarbitone induced sleep time and bromosulphalein retention. Propolis extract
showed significant improvement in the activity of both enzymes and suppressed toxicant induced increase in sleep time and
bromosulphalein retention. Choleretic activity of liver did not show any sign of toxicity after propolis treatment at a dose
of 200 mg/kg (id). Histopathological evaluation of the liver revealed that propolis reduced the incidence of liver lesions
including hepatocyte swelling and lymphocytic infiltrations induced by CCl4. Electron microscopic observations also showed improvement in ultrastructure of liver and substantiated recovery in biochemical
parameters. Protective activity of propolis at 200 mg/kg dose was statistically compared with positive control silymarin (50 mg/kg,
po), a known hepatoprotective drug seems to be better in preventing hepatic CYP 2E1 activity deviated by CCl4. These results lead us to speculate that propolis may play hepatoprotective role via improved CYP 2E1 activity and reduced
oxidative stress in living system. 相似文献
19.
《Bioscience, biotechnology, and biochemistry》2013,77(4):656-661
This study elucidated the effects of cornuside on carbon tetrachloride (CCl4)-induced hepatotoxicity. Rats were treated intraperitoneally with 0.5 mL/kg of CCl4. Sixteen h after CCl4 treatment, the levels of serum aminotransferases, tumor necrosis factor-α (TNF-α), and lipid peroxidation were significantly elevated, whereas the hepatic antioxidative enzyme activities were decreased. These changes were attenuated by cornuside. Histological studies also indicated that cornuside inhibited CCl4-induced liver damage. Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were elevated after CCl4 treatment, while cytochrome P450 2E1 (CYP2E1) expression was suppressed. Cornuside treatment inhibited the formation of liver nitrite, and reduced the overexpression of iNOS and COX-2 proteins, but restored the liver CYP2E1 content as compared with the CCl4-treated rats. Our data indicate that cornuside protects the liver from CCl4-induced acute hepatotoxicity, perhaps due to its ability to restore the CYP2E1 function and suppress inflammatory responses, in combination with its capacity to reduce oxidative stress. 相似文献
20.
J A Castro C R De Castro N D'Acosta M I Diaz Gomez E C De Ferreyra 《Biochemical and biophysical research communications》1973,50(2):273-279
The irreversible binding of14C from14CCl4 to microsomal lipids is decreased in animals treated with 3-methylcholantrene (3-MC), while it is increased in animals induced with phenobarbital (PB). CCl4-induced lipid peroxidation in 3-MC treated rats is as intense as in controls. Destruction of glucose 6-phosphatase (G6P-ase) by CCl4 is smaller in 3-MC treated rats than in controls. Destruction of total cytochrome P-450 (P-450 + P1-450) by CCl4 is smaller in 3-MC treated than in PB treated rats but similar to that obtained in controls. Results would indicate that P-450 would participate in CCl4 activation much more effectively than P1-450. 相似文献