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Since most infectious diseases can develop into sepsis, it is still a major medical problem. Some in-vivo studies showed promising properties of fluoxetine in the treatment of infections. This study aims the antimicrobial effect of fluoxetine on the inflammatory process used in the treatment of sepsis-modeled rats. Besides, to investigate the efficacy of fluoxetine on modifying the antibiotic effect of imipenem in the inflammatory response. An experimental sepsis model was divided into negative control, positive control, fluoxetine 5 mg/kg, imipenem 60 mg/kg, and combined (fluoxetine; imipenem). Procalcitonin (PCT), high-sensitivity C-reactive protein (hs-CRP), lactate, myeloperoxidase activity (MPO), the inflammation markers interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alfa (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) levels were measured by enzyme-linked immunosorbent assay method. Oxidative stress markers, total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), and native thiol (NT) were measured using photometric methods. Oxidative stress index (OSI) was calculated according to TAS and TOS levels. The statistical analysis was performed by Statistical Package for Social Sciences version 22.0. After treatment with fluoxetine, imipenem, and combined groups, IL-1β, IL-6, TNF-α, MPO activity, MCP-1, hs-CRP, PCT, lactate, and the oxidative stress markers OSI, and disulfide levels were decreased (p < 0.05). The TT, NT, and TAS levels significantly statistically increased (p < 0.05). This research demonstrates that fluoxetine has effects as anti-inflammatory and antioxidant, and the combined treatment with antibioticum imipenem indicates positive synergistic effects in the experimental sepsis model., (© 2022 Wiley Periodicals LLC.)

Background: We aimed to evaluate the optical coherence tomography(OCT) findings and oxidative stress parameters in patients with bipolar disorder(BD) and their unaffected first-degree relatives(FDRs) and to explore OCT findings and oxidative stress parameters as potential endophenotype candidates., Methods: Fifty patients with BD, 40 FDRs of BD, and 50 healthy controls(HCs) were included. OCT was performed to measure peripapillary retinal nerve fiber layer(RNFL), ganglion cell layer(GCL), inner plexiform layer(IPL), central macular, and minimum foveal thicknesses(CMT and MFT), choroidal thickness(ChT). 4-hydroxy-2-nonenal(HNE), total thiol(TT), native thiol(NT), total oxidant status(TOS), total antioxidant status(TAS), disulfide(DIS) and oxidative stress index(OSI) were measured from serum samples., Results: TOS was higher patients with BD and FDRs than HCs (p < .001 and p = .012, respectively). OSI, DIS, HNE levels were higher patients with BD and FDRs than HCs (p < .001). TAS, TT, NT levels were lower patients and FDRs than HCs (p < .001). MFT of patients was thinner than HCs (p = .001). CMT of patients was thinner than HCs (p = .006); the same trend was observed in FDRs but did not reach the statistical significance level (p = .07). The groups did not differ on RNFL and choroidal thickness or GCL and IPL volume., Limitations: Evaluation of only a few retinal layers., Conclusions: TOS, TAS, OSI, TT, NT, DIS, HNE can be useful endophenotype biomarkers in BD. Among the OCT findings, CMT was determined as the closest parameter to being an endophenotype biomarker. Our study corroborates that oxidative stress parameters are more effective than OCT findings in endophenotype studies., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Recently fragmented QRS (fQRS) on electrocardiography (ECG) has been introduced as a predictor of myocardial scarring and myocardial ischemia in coronary artery disease (CAD)., Objective: The aim of this study was to investigate the relationship between fQRS and fractional flow reserve (FFR) results in patients with the intermediate degree of coronary artery stenosis., Methods: A total of 301 consecutive patients who underwent coronary angiography (CAG) and FFR measurement for intermediate coronary artery stenosis were included in the study. The study patients were divided into two groups: the low FFR group (FFR value of ≤0.80) and normal FFR (FFR value of >0.80) group. Both groups were compared in terms of the presence of fQRS., Results: Of 301 patients, fQRS was detected in 128 (42.5%) and low FFR was detected in 115 (38.2%). In the low FFR group, fQRS was significantly higher (P<0.001). Multivariate analysis showed that fQRS was an independent predictor of myocardial ischemia in patients with intermediate coronary stenosis (OR=7.202, CI 95%, 4.195-12.367; p<0.001). The presence of fQRS had 70% sensitivity and 74% specificity for the prediction of FFR≤0.80., Conclusion: In clinical practice, the presence of fQRS on ECG is associated with myocardial ischemia in patients with intermediate coronary stenosis., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The polymorphic ventricular tachycardia (PVT) is uncommon arrhythmia with multiple causes and has been classified according to whether they are associated with long QT interval or normal QT. Whereas "Torsade de pointes (TdP)" is an uncommon and distinctive form of PVT occurring in a setting of prolonged QT interval, which may be congenital or acquired (congenital or acquired), "PVT with normal QT" is associated with myocardial ischemia, electrolyte abnormalities (hypokalemia), mutations of the cardiac sodium channel (Brugada syndrome), and the ryanodine receptor (catecholaminergic PVT). This distinction is crucial because of the differing etiologies and management of these arrhythmias. Moreover, the PVT in the setting of acute MI generally occurs during the hyperacute phase, is related to ischemia ("ischemic PVT") and is not associated with QT prolongation. It is triggered by ventricular extrasystoles with very short coupling interval (the "R-on-T" phenomenon) and is not pause-dependent. However, recently there has been described a new PVT during the "healing phase" of MI in patients with no evidence of ongoing ischemia and following excessive QT prolongation, the electrophysiologic abnormality being a "pause-dependent infarct-related TdP" due to a LQTS in healing MI patients. Therefore, "ischemic PVT" differs from "infarct-related TdP" in terms of pathophysiology and ECG manifestations., (Copyright © 2015 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.)

Objective: An increasing number of studies indicate that pepsin and bile acid cause damage to the ear, nose, and throat structures as a result of extraesophageal reflux. The aim of this study was to evaluate and compare the damaging effect of bile acids and pepsin on the middle ear mucosa., Material and Methods: Twenty-nine healthy rats were included in this study. The animals were divided into 5 groups. A single daily dose of 40 μmol/L chenodeoxycholic acid, 40 μg/mL pepsin, and saline were injected separately into the right middle ear of the rats. On day 30, all rats were decapitated, and formalin-fixed, paraffin-embedded samples of the middle ear both from the control and experimental rats were prepared. A semiquantitative analysis was performed., Results: Inflammatory response was seen in all middle ear mucosa of rats except control group 1. The degree of inflammatory response was higher in the bile acid group when compared with the other groups. Epithelial metaplastic changes with varying number of goblet cells were observed in both the bile acid- and pepsin-injected groups. These metaplastic changes were also higher in the bile acid-induced group than in the pepsin-injected group., Conclusions: This is the first study on the middle ear mucosal damage of both pepsin and bile acid. Our results demonstrate that bile acids were associated with more extensive mucosal injury at pH 7 in comparison to pepsin in a rat animal model. Inflammatory response and metaplastic changes may play an important role in the etiology of middle ear pathologies.

Coronary artery anomalies are detected on approximately 1.3% of coronary angiograms. Single coronary artery anomaly (SCA) is defined as the coronary artery arising from a single coronary ostium, nourishing the entire heart. SCA anomalies are usually benign; however, serious complications such as sudden cardiac death and myocardial infarction resulting from these anomalies are also reported in the literature. We report the anomalous origin of the right coronary artery (RCA) as a continuum of the septal branch from the left anterior descending (LAD) artery, which is a very rare variation of a single coronary artery.

In this paper, we will report a combined experimental and theoretical investigation of the molecular structure and spectroscopic parameters (FT-IR, (1)H NMR, (13)C NMR) of 5-benzoyl-4-phenyl-2-methylthio-1H-pyrimidine. The compound crystallizes in the triclinic space group P-1 with Z=2. The molecular geometry was also optimized using density functional theory (DFT/B3LYP) method with the 6-311G(d,p) and 6-311++G(d,p) basis sets in ground state and compared with the experimental data. All the assignments of the theoretical frequencies were performed by potential energy distributions using VEDA 4 program. Information about the size, shape, charge density distribution and site of chemical reactivity of the molecules has been obtained by mapping electron density isosurface with electrostatic potential (ESP). Also, non-linear optical properties of the title compound were performed at B3LYP/6-311++G(d,p) level. The theoretical results showed an excellent agreement with the experimental values., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objective: latrogenic femoral pseudoaneurysm is a well-known vascular access site complication. Many invasive and noninvasive techniques have been proposed for the management of this relatively common complication. In this study, we aimed to evaluate efficiency and safety of stethoscope-guided compression as a novel noninvasive technique in the femoral pseudoaneurysm treatment., Methods and Results: We prospectively included 29 consecutive patients with the diagnosis of femoral pseudoaneurysm who underwent coronary angiography. Patients with a clinical suspicion of femoral pseudoaneurysm were referred to colour Doppler ultrasound evaluation. The adult (large) side of the stethoscope was used to determine the location where the bruit was best heard. Then compression with the paediatric (small) side of the stethoscope was applied until the bruit could no longer be heard and compression was maintained for at least two sessions. Once the bruit disappeared, a 12-hour bed rest with external elastic compression was advised to the patients, in order to prevent disintegration of newly formed thrombosis. Mean pseudoaneurysm size was 1.7 +/- 0.4 cmx 3.0 +/- 0.9 cm and the mean duration of compression was 36.2 +/- 8.5 minutes.Twenty-six (89.6%) of these 29 patients were successfully treated with stethoscope-guided compression. In 18 patients (62%), the pseuodoaneurysms were successfully closed after 2 sessions of 15-minute compression. No severe complication was observed., Conclusion: Stethoscope-guided compression of femoral pseudoaneurysms is a safe and effective novel technique which requires less equipment and expertise than other contemporary methods.

The occurrence of cryptic and pseudocryptic species, often living in sympatry, is widespread among microalgae. This phenomenon raises important questions about niche partitioning between these closely related species. To date, however, few studies have addressed the ecological mechanisms underlying sympatry in cryptic and pseudocryptic species. As a result, we have only a limited understanding of the factors that govern their distribution along environmental gradients. Here, we used the ribosomal internal transcribed spacer (ITS), 18S rRNA gene, and the RUBISCO LSU (rbcL) chloroplast gene sequence data together with cell wall morphology to show that estuarine populations of the widespread and common benthic diatom Navicula phyllepta Kütz. consist of pseudocryptic species. Growth rate measurements in function of salinity showed that N. phyllepta strains assigned to the different species differed in their tolerance to low salinities (<5 practical salinity units, psu), which was reflected by their different (but widely overlapping) distribution in the Westerschelde estuary (the Netherlands). Multiple regression analyses of the factors determining the abundance of the different species in field samples revealed that, in addition to salinity, sediment type and ammonium concentrations were probably equally important. Our results show that N. phyllepta sensu lato comprises different species with specialized ecophysiological characteristics rather than generalists with a broad adaptability to different environmental conditions., (© 2009 Phycological Society of America.)

Background: Various caspases have been implicated in the development of secondary damage after spinal cord injury (SCI). Anticaspase therapy that targets only one caspase has been investigated in a variety of in vitro and in vivo studies. This study examined the neuroprotective effects of Q-VD-OPh, a pan-caspase inhibitor, in a rat model of SCI., Methods: Thirty Wistar albino rats were divided into 3 groups of 10 each: the sham-operated controls (group 1), the trauma-created controls (group 2), and the QVD- OPh-treated rats (group 3). An SCI (a trauma of 40 g-cm) was produced at the thoracic level (T8-T10) by the weight-drop technique. The response to injury and the neuroprotective effects of Q-VD-OPh were investigated by histopathologic examination and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) 24 hours and 5 days after trauma. The inclined plane technique of Rivlin and Tator and a modified version of Tarlov's grading scale were used to assess the functional status of the rats 24 hours, 3 days, and 5 days after injury., Results: Twenty-four hours after trauma, light microscopic examination of a specimen taken from group 2 rats revealed hemorrhage, necrosis, vascular thrombi, and edema. Group 3 tissue samples showed similar features at that time. Twenty-four hours after trauma, the mean apoptotic cell number was 4.47 +/- 0.35 cells in group 2 and 1.58 +/- 0.33 in group 3. Five days after injury, the mean apoptotic cell count was 4.35 +/- 0.47 in group 2 and 1.25 +/- 0.34 in group 3. Thus the number of TUNEL-positive cells in an injured spinal cord was greatly reduced by treatment with Q-VDOPh. The neurologic function scores (both the inclined plane performance and motor grading scores) were significantly better in the Q-VD-OPh-treated group than in the trauma-created control group., Conclusion: The marked antiapoptotic properties of Q-VD-OPh due to the inhibition of all caspases render it a promising novel agent. A therapeutic strategy using Q-VD-OPh may eventually lead to the effective treatment of SCI in humans.

Background: In cases of trauma to the left renal vein (LRV), its ligation near the inferior vena cava (IVC) is considered, but the consequences are not always good. We investigated the role of collateral venous drainage after ligation of the LRV by studying the renal function and histology after ligation of the LRV near the IVC alone or with ligation of the gonadal or adrenal collaterals, in right-nephrectomized (RN) rats., Material and Methods: Ligation of the LRV near the IVC alone (group 1) or with ligation of the adrenal (group 2) or gonadal (group 3) collaterals was studied in RN Wistar rats (n=18 per group). The renal histopathology (ischemic cortical necrosis) and functional status (urea, creatinine, sodium, and potassium) were compared., Results: In RN rats, the results were better when ligating the LRV near the IVC alone or with the adrenal collaterals [mortality 4/18 (22.2%) and 3/18 (16.7%), respectively] than when ligating the LRV near the IVC plus the gonadal collaterals [mortality 15/18 (83.3%)] (p<0.0001). All early deaths occurred within three days and resulted from serious histopathological (ischemic cortical necrosis) and functional (increased urea, creatinine, and potassium; decreased sodium) renal damage., Conclusion: In right-nephrectomized rats, the LRV near the IVC and the adrenal collateral can be ligated, while the gonadal collateral should be preserved.

Background: An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. In this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model., Methods: Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma., Findings: Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotic cell numbers in groups 1 and 2 were zero and 4.57 +/- 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 +/- 0.34 cells, a value significantly lower than that in group 2 (P < .05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05)., Conclusions: AK 295 inhibited apoptosis via calpaindependent pathways and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI.

Apoptosis is an important element of the secondary processes that occur after spinal cord injury. Calpain and caspases are key proteases in apoptotic cell death. We evaluated the neuroprotective effects of SJA6017 (a calpain inhibitor) and measured functional recovery in a rat spinal cord injury model. Thirty Wistar albino rats were divided into three groups of 10 animals each: sham-operated (group 1), trauma control (group 2) and trauma-plus-SJA6017 treatment (group 3). Spinal cord trauma was produced in the thoracic region of the animals. Rats in group 3 received SJA6017 1 min after trauma. Treatment efficacy was evaluated after injury using light microscopy and TUNEL staining. Neurological performance was assessed using an inclined plane and a modified version of the Tarlov's grading scale. Group 2 rats showed moderate trauma with widespread edema, hemorrhage, vascular thrombi and necrosis 24 h after injury. Group 3 rats had significantly reduced tissue injury and apoptosis. Tarlov scores revealed that group 3 rats also had ameliorated recovery of limb function. Our results demonstrate that treatment with SJA6017 reduces apoptotic cell death, preserves spinal cord tissue and improves functional outcome. Treating calpain-induced apoptosis with this agent may be a feasible therapeutic strategy for patients with spinal cord injury.

We investigated the therapeutic efficacy of Ac-DMQD-CHO, a caspase-3 inhibitor, and functional recovery in spinal cord injury in a rat model. Thirty rats were randomized into three groups of 10 each. In groups 2 and 3, spinal cord trauma was produced in the thoracic region. Group 3 rats were treated with Ac-DMQD-CHO. Treatment responses were evaluated based on histopathological and TUNEL staining findings at 24 h and 5 days post-injury. Neurologic performance was assessed during and following treatment. Twenty-four hours after injury, light microscopy examination revealed diffuse hemorrhagic necrosis, edema, vascular thrombi, and polymorphonuclear leukocyte infiltration in group 2 and 3 rats, but cavitation and demyelinization were less prominent in group 3. At this time point, treatment of the rats with Ac-DMQD-CHO significantly reduced the number of apoptotic cells. Traumatic injury to the spinal cord causes apoptosis and administration of Ac-DMQD-CHO decreases apoptosis and improves functional outcome.

Background: Apoptosis as a cell death mechanism is important in numerous diseases, including traumatic SCI. We evaluated the neuroprotective effects of Ac.YVAD.cmk and functional outcomes in a rat SCI model., Methods: Thirty rats were randomized into 3 groups of 10: sham-operated, trauma only, and trauma plus Ac.YVAD.cmk treatment. Trauma was produced in the thoracic region by a weight-drop technique. Group 3 rats received Ac.YVAD.cmk (1 mg/kg, ip) 1 minute after trauma. The rats were killed at 24 hours and 5 days after injury. Efficacy was evaluated with light microscopy and TUNEL staining. Functional outcomes were assessed with the inclined plane technique and a modified version of the Tarlov grading system., Results: At 24 hours postinjury, the respective mean number of apoptotic cells in groups 1, 2, and 3 were 0, 5.26 +/- 0.19, and 0.97 +/- 0.15. Microscopic examination of group 2 tissues showed widespread hemorrhage, edema, necrosis, and polymorphic nuclear leukocyte infiltration and vascular thrombi. Group 3 tissues revealed similar features, but cavitation and demyelination were less prominent than those in group 2 samples at this period. At 5 days postinjury, the respective mean inclined plane angles in groups 1, 2, and 3 were 65.5 +/- 2.09, 42.00 +/- 2.74, and 52.5 +/- 1.77. Motor grading of animals revealed a similar trend. These differences were statistically significant (P < .05)., Conclusions: Ac.YVAD.cmk inhibited posttraumatic apoptosis in a rat SCI model. This may provide the basis for development of new therapeutic strategies for the treatment of SCI.

Greater clinical understanding of the pivotal role of apoptosis in spinal cord injury (SCI) has led to new and innovative apoptosis-based therapies for patients with an SCI. Tauroursodeoxycholic acid (TUDCA) is a biliary acid with antiapoptotic properties. To our knowledge, this is the first study in the English language to evaluate the therapeutic efficacy of TUDCA in an experimental model of SCI. Thirty rats were randomized into three groups (sham-operated, trauma only, and trauma plus TUDCA treatment) of 10 each. In groups 2 and 3, spinal cord trauma was produced at the T8-T10 level via the Allen weight drop technique. Rats in group 3 were treated with TUDCA (200 mg/kg intraperitoneal) 1 min after trauma. The rats were killed either 24 h or 5 days after injury. The neuroprotective effect of TUDCA on injured spinal cord tissue and the effects of that agent on the recovery of hind-limb function were assessed. The efficacy of treatment was evaluated with histopathologic examination and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) analysis. Histopathologic characteristics were analyzed by comparison of hematoxylin-and-eosin stained specimens. Neurologic evaluations were performed 24 h, 3 days, and 5 days after trauma. Hind-limb function was assessed with the inclined plane technique of Rivlin and Tator and the modified version of Tarlov's grading scale. Twenty-four hours after injury, there was a significantly higher number of apoptotic cells in the lesioned spinal cord group than in the sham-operated control group. Treatment of the rats with TUDCA significantly reduced the number of apoptotic cells (4.52+/-0.30 vs. 2.31+/-0.24 in group 2) and the degree of tissue injury. Histopathologic examination showed that group 3 rats had better spinal cord architecture compared with group 2 rats. Five days after injury, the mean inclined plane angles in groups 1, 2, and 3 were 65.50 degrees +/- 2.09, 42.00 degrees +/- 2.74, and 53.50 degrees +/- 1.36. Motor grading of the rats revealed a similar trend. These differences were statistically significant (p<0.05). The mechanism of neuroprotection in the treated rats, although not yet elucidated, may be related to the marked antiapoptotic properties of TUDCA. A therapeutic strategy using TUDCA may eventually lead to effective treatment of SCI without toxic effects in humans.

The diversity and spatio-temporal distribution of ammonia-oxidizing Archaea (AOA) and Bacteria (AOB) were investigated along a salinity gradient in sediments of the Westerschelde estuary. Sediment samples were collected from three sites with different salinities, and at six time points over the year. Denaturing gradient gel electrophoresis of PCR-amplified 16S rRNA and amoA gene fragments was used to identify the AOA and AOB present. Members of the AOA were mainly belonging to the Crenarchaeota Group 1, which were found at all sites, while members of the genus Nitrosomonas, which were abundant at the brackish sites, and of the genus Nitrosospira, which were present in early spring at the marine sites, were found to be the dominant AOB. Statistical analysis indicated that salinity and temperature were the main factors controlling the diversity and distribution of both AOA and AOB. Variability in net primary production rates was also correlated with species composition of both groups, but changes in the nitrite concentration only to the distribution of the AOA.

Stellate cells are activated by free radicals, and synthesize collagen. N-acetylcysteine (NAC) is a precursor of reduced glutathione and a potent scavenger of hydroxyl radicals and has potential antifibrotic effects. We aimed to test the effects of NAC on bile duct ligation (BDL) induced liver damage in rats. Forty-seven Wistar rats were divided into 5 groups: group 1, BDL+NAC (n=10); group 2, BDL (n=10); group 3, sham+NAC (n=10); group 4, sham (n=10); and group 5, control group (n=10). NAC (50 micromol/kg per day) or saline of single doses were administered intraperitoneally for 28 days. Serum biochemical and liver oxidative stress parameters were studied. Liver collagen level was determined by the method of Lopez de Leon and Rojkind. Liver slides were stained by hematoxylin and eosin and Masson trichrome\Gomory reticulum staining. Aspartate aminotransferase (AST) and alkaline phosphatase levels in the BDL+NAC group were lower than the BDL group and were higher than the control groups (all P< .001). Malondialdehyde, luminal, and glutathione levels in group 1 were lower than the BDL group (P= .01, P= .002, and P< .001) and higher than the control groups (all P< .001). NAC had no effect on alanine aminotransferase (ALT), gammaglutamyl transferase, bilirubin, albumin, or lucigenin levels. Liver collagen levels were higher in the BDL groups (P< .001); however, NAC had no effect on the collagen levels. The BDL groups showed stage 3 fibrosis; all the control groups were normal. NAC improved some biochemical parameters (AST, alkaline phosphatase) and oxidative stress parameters (malondialdehyde, luminol, glutathione) in the BDL model. NAC was found to be effective on cholestasis-induced hepatotoxicity. However, NAC was inefficient as an antifibrotic agent within a 1-month period of administration in the BDL model.