Therapeutic Effects Of Thymoquinone Research Articles

The therapeutic effect of thymoquinone on methotrexate induced ovarian toxicity in adult female albino rats.

The therapeutic effect of thymoquinone on methotrexate induced ovarian toxicity in adult female albino rats.

Continuous Thymoquinone Administration Mitigates Sodium Iodate-Induced Retinal Degeneration in Rats

Purpose This study aimed to investigate the protective or therapeutic effect of thymoquinone (TQ) in a retinal degeneration rat model and its relationships with the retina ultrastructure, heme oxygenase 1 (HO-1), caspase-3, and RPE65 expressions and to determine whether TQ has a therapeutic effect at the biochemical level. Methods A total of 25 adult Wistar albino rats were divided into the following treatment groups: saline (control: CONT), CO (corn oil), sodium iodate (SI), TQ + SI, and SI + TQ injection groups. Retina morphology, RPE65, HO-1, and caspase-3 expression levels were evaluated using immunohistochemistry, and optical density was determined using ImageJ. Ultrastructural evaluations were performed with electron microscopy. Thiol-disulfide homeostatic parameters were examined in serum samples. Results Outer nuclear layer (ONL) thickness was significantly higher in the SI + TQ group compared to the SI group. The RPE65 expression significantly decreased in the SI group compared with the CONT and CO groups. A significant increase in RPE65 expression level and a significant decrease in caspase-3 expression level were found in the SI + TQ group compared with the SI group. The increase in HO-1 expression level was significantly higher in the TQ treatment groups, particularly in the SI + TQ group. In the SI and TQ + SI groups, the ONL thickness significantly decreased with a significant increase in caspase-3 expression compared to the CONT and CO groups. In the treatment groups, decreased organelle damage was observed on electron microscopy. In the SI + TQ group, the disulfide/native thiol and disulfide/total thiol ratios were significantly lower than all other groups, while the native/total thiol ratio was significantly higher than the other experimental groups. Conclusions The present study provides evidence that continuous TQ treatment can increase HO-1 and RPE65 expression and decrease apoptosis (caspase-3 levels), thereby preserving the retina at the ultrastructural level. Moreover, TQ administration can maintain thiol/disulfide homeostasis in SI-induced retinal degeneration-modelled rats.

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats.

Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein(GFAP), Cas-3, and nervegrowth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition,malondialdehyde (MDA), superoxide dismutase(SOD), and catalase(CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

Chemopreventive and therapeutic efficacy of thymoquinone on experimentally induced hamster buccal pouch carcinogenesis

Aim: The present study aimed to investigate the chemopreventive and therapeutic effect of thymoquinone (TQ) on experimentally induced hamster buccal pouch carcinogenesis. Methodology : 40 Syrian male hamsters were classified into 4 equal groups (G(s)) of 10 each. GI: The animals remained untreated. The pouches of animals in GII, GIII, and GIV were painted 3 times a week for 14 weeks (ws). with 7,12-dimethylbenz (a) anthracene (DMBA). GII: No additional treatment was administered. Those in GIII: oral administration of TQ at a dose of 30 mg kg-1, one week before, as well as, during the application of DMBA on alternate days for 14 ws, whereas in GIV: The animals were injected intraperitoneally (IP) with TQ 50 mg/kg body weight thrice a week for 3ws. After the end of the experiment, the gross observations were made. Then, the fresh pouch specimens were surgically bisected into two pieces, one for Hematoxylin and Eosin (H&E) stain and immunohistochemistry (IHC) stain using Bcl-2. The other piece was used for apoptosis detection through a flow cytometry (FCM) test. Results: Gross observation showed variation in reduction of the tumor size in chemoprevention and treated group compared to the DMBA treated group.

Thymoquinone modulates the expression of sepsis-related microRNAs in a CLP model.

Sepsis is a clinical syndrome common in critical care settings. In the present study, the therapeutic effect of thymoquinone (TQ) on the expression of sepsis-related microRNAs (miRNAs/miRs), levels of inflammatory markers, organ dysfunction and mortality were investigated in a cecal ligation and puncture (CLP) rat model. A single dose of TQ (1 mg/kg) was administered to animals 24 h after CLP and the mortality rate was assessed up to 7 days following the induction of sepsis. In addition, blood samples were collected at different time points and the expression levels of miRNAs (i.e. miR-16, miR-21, miR-27a and miR-34a) were examined, along with the levels of inflammatory cytokines (i.e. TNF-α, IL-1α, IL-2, IL-6 and IL-10) and sepsis markers (i.e. C-reactive protein, endothelial cell-specific molecule-1, VEGF, procalcitonin and D-dimer). Liver, kidney and lung tissues were also collected for further histological examination. Treatment with TQ significantly downregulated the miRNA expression levels, as well as the levels of inflammatory cytokines and early-stage sepsis biomarkers by 30-70% at 12-36 h (P<0.05). Furthermore, CLP model rats treated with TQ exhibited an ~80% increase in survival rate compared with that in the untreated CLP group. In addition, TQ induced the preservation of organ function and structure. In conclusion, the present study demonstrated a promising therapeutic effect of TQ against the sequelae of sepsis.

Therapeutic effect of Thymoquinone on behavioural response to UCMS and neuroinflammation in hippocampus and amygdala in BALB/c mice model.

Major depressive disorder is the leading cause of disability worldwide. The corticolimbic system plays a critical role in the emotional and cognitive aspects of major depressive disorder. Owing to the unsatisfactory efficacy of conventional antidepressants, there is a need to explore novel therapies. The current study aimed to explore the antidepressant potential of thymoquinone, a natural compound with anti-inflammatory activity, and propose its underlying mechanism of action in the unpredictable chronic mild stress (UCMS) mouse model. Coat state, forced swim test, elevated plus maze test, novelty suppressed feeding test and social interaction test were performed to quantify the behavioural shift induced by UCMS and the effect of thymoquinone and fluoxetine treatment. In addition, messenger RNA (mRNA) expression levels of inflammatory cytokines (IL-1β, IL-6 and TNF-α) and BDNF and NeuN were analysed by a quantitative real-time polymerase chain reaction in the hippocampus and amygdala of experimental and control groups. UCMS significantly deteriorated coat state. Thymoquinone reinstated the resignation behaviour and latency to feed affected by UCMS. UCMS induced an increase in inflammatory cytokines (IL-1β, IL-6 and TNF-α) in the hippocampus and amygdala, which was decreased by thymoquinone. UCMS caused an increase in BDNF and NeuN mRNA levels in the amygdala while a decrease in the hippocampus. This opposite effect on BDNF was also compensated by thymoquinone; however, thymoquinone did not significantly change Ki67 and NeuN mRNA levels in the hippocampus. Thymoquinone restored the behavioural changes induced by UCMS. In addition, the antidepressant effect of thymoquinone is in line with changes in inflammatory parameters and changes in BDNF in the hippocampus and amygdala.

Therapeutic effects of thymoquinone in doxorubicin-induced hepatotoxicity via oxidative stress, inflammation and apoptosis.

Cancer is a lethal disease that is characterized by uncontrolled cell division and proliferation, and it results in death in many organisms. Doxorubicin (DOX) is a therapeutic agent used for treatment of many cancer types, but it induces serious hepatotoxicity. In this study, we aimed to determine possible hepato-therapeutic effects of thymoquinone (THQ) on DOX-induced hepatotoxicity in rats. Rats were divided into five groups (n=8): Control, THQ (10mg/kg/day/i.p for 14days), Olive Oil (equal volume with THQ for 14days), DOX (single dose, 15mg/kg/i.p on 7th day) and DOX+THQ (10mg/kg/day/i.p and DOX 15mg/kg/i.p on 7th day). At the end of the experiment, liver tissues were extracted and evaluated histopathologically. eNOS, iNOS and Cas-3 immunostaining were performed to determine the expression levels. TUNEL method was used to determine apoptotic index. Furthermore, liver tissue total antioxidant status (TAS), total oxidant status (TOS), TNF-α and TGF-β levels were measured by ELISA assay. The DOX group showed histopathological deterioration compared to Control group. Moreover, apoptotic index, eNOS, iNOS and Cas-3 expressions increased in DOX group. While TAS level of the DOX group decreased, TOS level increased. TNF-α and TGF-β levels increased in DOX group. However, there was improvement in DOX+THQ group compared to DOX group. Moreover, apoptotic cell number, eNOS, iNOS and Cas-3 expressions decreased in DOX+THQ group compared to DOX group. We concluded that thymoquinone can be used as a phytotherapeutic for reducing DOX-induced liver damage.

Therapeutic effects of thymoquinone or capsaicin on acrylamide-induced reproductive toxicity in rats mediated by their effect on oxidative stress, inflammation, and tight junction integrity

In the field of environmental toxicology, endocrine-disrupting effects have become a major concern. The present research set out to investigate the possible reproductive toxicity of acrylamide. The research was also expanded to explore the protective effects of two nutraceuticals, thymoquinone (TQ) and capsaicin, against acrylamide-induced reproductive toxicity. Six groups of sixty male albino rats were created. Group 1 was used as a control. Rats were administered a daily dose of acrylamide and acted as the model in Group 2. TQ was provided to rats once a day in Group 3. Capsaicin was administered to rats once a day in Group 4. TQ was given once daily to rats exposed to acrylamide in Group 5. Rats were given capsaicin once a day for eight weeks after being exposed to acrylamide in Group 6. Acrylamide induced oxidative stress, testicular NF-κB/p65 expression, and down-regulated the expression of occludin, all of which can contribute to its testicular toxicity, while TQ or capsaicin removes all of these toxicity signs. TQ and capsaicin have shown efficacy in alleviating all of the acrylamide's toxic insults in the current reproductive toxicity model. Both nutraceuticals upregulated the expression of occludin in testicular tissue and restored tight junction integrity, in addition to their well-known antioxidant and anti-inflammatory effects, which were confirmed in this study.

Protective Effects of Thymoquinone, an Active Compound of Nigella sativa, on Rats with Benzo(a)pyrene-Induced Lung Injury through Regulation of Oxidative Stress and Inflammation.

Benzopyrene [B(a)P] is a well-recognized environmental carcinogen, which promotes oxidative stress, inflammation, and other metabolic complications. In the current study, the therapeutic effects of thymoquinone (TQ) against B(a)P-induced lung injury in experimental rats were examined. B(a)P used at 50 mg/kg b.w. induced lung injury that was investigated via the evaluation of lipid profile, inflammatory markers, nitric oxide (NO), and malondialdehyde (MDA) levels. B(a)P also led to a decrease in superoxide dismutase (SOD) (34.3 vs. 58.5 U/mg protein), glutathione peroxidase (GPx) (42.4 vs. 72.8 U/mg protein), catalase (CAT) (21.2 vs. 30.5 U/mg protein), and total antioxidant capacity compared to normal animals. Treatment with TQ, used at 50 mg/kg b.w., led to a significant reduction in triglycerides (TG) (196.2 vs. 233.7 mg/dL), total cholesterol (TC) (107.2 vs. 129.3 mg/dL), and inflammatory markers and increased the antioxidant enzyme level in comparison with the group that was administered B(a)P only (p < 0.05). B(a)P administration led to the thickening of lung epithelium, increased inflammatory cell infiltration, damaged lung tissue architecture, and led to accumulation of collagen fibres as studied through haematoxylin and eosin (H&E), Sirius red, and Masson’s trichrome staining. Moreover, the recognition of apoptotic nuclei and expression pattern of NF-κB were evaluated through the TUNEL assay and immunohistochemistry, respectively. The histopathological changes were found to be considerably low in the TQ-treated animal group. The TUNEL-positive cells increased significantly in the B(a)P-induced group, whereas the TQ-treated group showed a decreased apoptosis rate. Significantly high cytoplasmic expression of NF-κB in the B(a)P-induced group was seen, and this expression was prominently reduced in the TQ-treated group. Our results suggest that TQ can be used in the protection against benzopyrene-caused lung injury.

Thymoquinone improves testicular damage and sperm quality in experimentally varicocele-induced adolescent rats.

The aim of this study was to investigate the protective and therapeutic effects of thymoquinone against the negative effects of varicocele on testicular tissue and sperm morphology. Five groups were formed by random selection from a total of 40 adult male Wistar rats (n=8). Thymoquinone (5mg/kg/day) was administered intraperitoneally to the varicocele-dimethyl sulfoxide-olive oil-thymoquinone (VT) group and the sham-thymoquinone group. At the end of the 60th day, all groups were anaesthetised and the left testis was removed from the body quickly. One half of the testis tissue, which was divided into two, was separated for biochemical and Western blot analysis, while the other half were fixed in Bouin's fixative. As a result of biochemical, molecular and histopathological analyses, a statistically significant increase was found in the varicocele group testicular tissues in the malondialdehyde level, apoptotic index, Bax expression, cytochrome c expression and Bax/Bcl-2 ratio compared with the sham group. In addition, histopathological changes characterised by partial or complete degeneration of the germinal epithelium were observed in the seminiferous tubules in the same group. Total oxidant status level and sperm count with abnormal morphology increased in varicocele group, whereas total antioxidant status level decreased. In the VT group, all of the biochemical, molecular and histopathological changes detected in the varicocele group were statistically significantly reduced. When the findings obtained in this study are evaluated, it can be said that thymoquinone has the potential to be used as a preventive and therapeutic pharmacological agent in the medical treatment of varicocele. Although the exact mechanism of action of thymoquinone has not been fully elucidated, the findings obtained in this study support the view that thymoquinone showed a cytoprotective effect by reducing apoptosis, oxidative stress and lipid peroxidation.

Biological and therapeutic activities of thymoquinone: Focus on the Nrf2 signaling pathway.

Thymoquinone is a monoterpenoid compound, which is derived from volatile and fixed oil of Nigella sativa (Ranunculaceae). This phytochemical compound has several biological effects, including antioxidant, antibacterial, antineoplastic, nephroprotective, hepatoprotective, gastroprotective, neuroprotective, anti-nociceptive, and anti-inflammatory activities. Thymoquinone shows pharmacological activities, including anti-hepatocellular carcinoma, nephroprotection, neuroprotection, retina protection, gastroprotection, cardioprotection, anti-allergy, reproductive system protection, bladder protection, and respiratory protection. It was found that these beneficial effects are mostly related to modulation of the Nrf2 signaling pathway by blockage of Keap1, stimulating the expression of the Nrf2 gene, and inducing the nuclear translocation of Nrf2. In the present review, the therapeutic effects of thymoquinone are overviewed through the Nrf2 signaling pathway.

Thymoquinone is a protective agent that reduces the negative effects of doxorubicin in rat testis.

Doxorubicin (DOX) is used for treatment of many cancer types. Thymoquinone (THQ) is a powerful antioxidant agent used for reducing side effects of several drugs. The aim of this study is to determine possible therapeutic effects of THQ on doxorubicin-induced testicular toxicity in rats. Rats were divided into five groups (n = 8): control, THQ, olive oil, DOX (a single dose of 15 mg/kg intraperitoneally (i.p.) on seventh day of the experiment), and DOX + THQ (10 mg/kg THQ per day and 15 mg/kg DOX i.p. on seventh day). Animals were euthanized, and testis tissues were evaluated histopathologically. Caspase 3 and HSP90 immunostaining were performed to determine the expression levels of these proteins among groups. Terminal deoxynucleotidyl transferase 2'-deoxyuridine, 5'-triphosphate nick-end labeling method was used for evaluation of apoptotic index. Moreover, serum testosterone levels and total antioxidant status (TAS) and total oxidant status (TOS) in testicular tissue were measured by ELISA assay. The DOX group had histopathological deterioration compared to the control group. There was an increase in apoptotic index, caspase 3 and HSP90 expressions in the DOX group. While TAS level of the DOX group decreased, TOS level increased when compared with the other groups. Serum testosterone levels in the DOX group decreased compared to the control group. However, there was improvement in testicular tissue in DOX + THQ group compared to the DOX group. There was a decrease in apoptotic index, caspase 3, and HSP90 expressions in DOX + THQ group compared to the DOX group. Testosterone level of DOX + THQ significantly increased compared to the DOX group. We suggest that THQ can be used as a protective agent to reduce the toxic effects of DOX.

Therapeutic effect of thymoquinone against lead-induced testicular histological damage in male Wistar rats.

Lead (Pb) is a nonthreshold multi-targeted toxicant that causes alterations in different organs of the body, especially the gonads. This study was aimed to investigate the possible protective effect of thymoquinone (TQ), the major active ingredient of volatile oil of Nigella sativa seeds, against Pb-induced testicular histological damage. Adult male rats were randomised into four groups as follows: control group received no treatment, Pb group was exposed to 2000ppm of Pb acetate in drinking water, Pb-TQ group was cotreated with Pb plus TQ (5mg/kg/day, per os) and TQ group receiving only TQ. All treatments were applied for five weeks. Results showed that Pb exposure produced morphological changes in the testis, especially degeneration of germinal epithelium, sloughing of germ cells into the lumen of seminiferous tubules and reduction in the number of luminal spermatozoa. Interestingly, coadministration of TQ to the metal-treated animals prevented the testicular adverse effects. In conclusion, our data indicate for the first time a remarkable protective effect of TQ against Pb-induced testicular histopathological lesions in rat. On this basis, TQ deserves more consideration and further examination as a potential therapeutic option.

Thymoquinone reduces mortality and suppresses early acute inflammatory markers of sepsis in a mouse model

BackgroundSepsis is a severe systemic condition caused by an excessive inflammatory response to microbial infections, which often results in high mortality. AimsIn the present study, the therapeutic effects of thymoquinone were investigated for Gram-negative bacteria-induced sepsis in mice. MethodsThymoquinone was administered as 1or 2 mg/kg intraperitoneally 2 h after Escherichia coli (E. coli) challenge. Animal morality was assessed up to 96 h post infection and inflammatory proteins levels were measured 6 h after thymoquinone treatment in various groups using enzyme-linked immunosorbent assay (ELISA) techniques. Key findingsThe E. coli inoculation markedly increased the level of plasma cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-2, IL-6 and IL-10. In addition, the levels of selected early sepsis biomarkers such as CRP, VEGF and ESM-1 were amplified in the septic group. Treatment with thymoquinone significantly downregulated the circulating concentrations of the inflammatory proteins (p < 0.05). In addition, ∼75% of mice in the thymoquinone (1 mg/kg) group survived at 96h of observation compared with ∼8% of the untreated group (p = 0.0016). SignificanceThe present results indicate that thymoquinone suppresses acute inflammatory responses induced by sepsis including early stage biomarkers and reduces sepsis-related mortality. These findings suggest that thymoquinone could be of a potential therapeutic value in the management of sepsis.

Potential therapeutic effects of thymoquinone on treatment of amphetamine abuse

Potential therapeutic effects of thymoquinone on treatment of amphetamine abuse

GC-MS-based Metabolomic Profiling of Thymoquinone in Streptozotocin-induced Diabetic Nephropathy in Rats

*Diabetic nephropathy is a common complication of diabetes mellitus and one of the major etiologies of end-stage renal disease. Specific therapeutic interventions are necessary to treat such complications. The present study was designed to investigate the metabolomic changes induced by thymoquinone for the treatment of diabetic nephropathy, using a rodent model. Rats were divided into three different groups (n = 6 each): control, diabetic, and thymoquinone- treated diabetic groups. Metabolites in serum samples were analyzed via gas chromatography-mass spectrometry. Multiple changes were observed, including those related to the metabolism of amino acids and fatty acids. The correlation analysis suggested that treatment with thymoquinone led to the reversal of diabetic nephropathy that was associated with modulations in the metabolism and proteolysis of amino acids, fatty acids, glycerol phospholipids, and organic acids. In addition, we explored the mechanisms linking the metabolic profiling of diabetic nephropathy, with a particular emphasis on the potential roles of increased reactive oxygen species production and mitochondrial dysfunctions. Our findings demonstrated that metabolomic profiling provided significant insights-into the basic mechanisms of diabetic nephropathy and the therapeutic effects of thymoquinone.

The therapeutic effect of thymoquinone on acoustic trauma-induced hearing loss in rats.

Thymoquinone has antioxidant properties. We hypothesized that thymoquinone may prevent or alleviate hearing loss induced by acoustic trauma. We aimed to study thymoquinone's effect on hearing function with distortion-product otoacoustic emissions and auditory brainstem response. Thirty adult Spraque Dawley rats were randomized into four groups following exposure to acoustic trauma for 4h. Control group (n=7) did not receive further treatment. Thymoquinone-20 (n=8) and Thymoquinone-40 (n=8) received 20 and 40mg/kg of intraperitoneal thymoquinone, respectively. Corn-oil group (n=7) received 1ml of corn oil intraperitoneally. Hearing function of both ears was tested with distortion-product otoacoustic emission and auditory brainstem response before, and shortly after acoustic trauma, and 96h following acoustic trauma. Post-trauma signal/noise ratios and wave V amplitude/latencies of all groups were significantly low compared with pre-trauma values, which indicate no preventive effect of thymoquinone. Rats in Thymoquinone-20 showed a significantly improved distortion-product otoacoustic emission and auditory brainstem response results at 4000 frequency and above in post-treatment tests (p<0.05). Improvement in Thymoquinone-40 at the same frequencies was insignificantly inferior to Thymoquinone-20, yet superior to control and corn-oil groups (p<0.05). We conclude that thymoquinone may not prevent acoustic trauma-induced hearing loss, however, at 20mg/kg for 96h, may repair the damage.

Thymoquinone effectively alleviates lung fibrosis induced by paraquat herbicide through down-regulation of pro-fibrotic genes and inhibition of oxidative stress.

The potential preventive and therapeutic effects of thymoquinone (TQ) and its molecular mechanism were evaluated in paraquat (PQ)-induced pulmonary fibrosis in mice. TQ was administered orally at the doses of 20 and 40mg/kg during the course and after development of fibrosis. Pathological changes, expressions of genes involved in fibrogenesis, hydroxyproline (HP) and oxidative stress parameters were determined in the lung tissues. TQ dose-dependently recovered the pathological changes induced by PQ. TQ decreased hydroxyproline content, lipid peroxidation and restored the antioxidant enzymes to the normal values. In molecular level, expressions of TGF-β1, α-SMA, collagen 1a1 and collagen 4a1 genes were also returned to the control level by TQ. This study indicated that TQ has the preventive and therapeutic potentials for the treatment of lung fibrosis by inhibition of oxidative stress and down-regulation of profibrotic genes.

Biochemical, Histopathological and Immunohistochemical Evaluation of the Protective and Therapeutic Effects of Thymoquinone against Ischemia and Ischemia/Reperfusion Injury in the Rat Ovary

Aim: To evaluate the antioxidant effects of thymoquinone (TQ) and to investigate the biochemical, histopathological and immunohistochemical changes in experimental rat ovarian torsion. Methods: A total of 48 female adult rats were used in this study and randomly divided into 7 groups: (1) sham operation; (2) bilateral 3-hour ovarian ischemia; (3) 3-hour ischemia and 3-hour reperfusion; (4) and (5) rats were administered 20 and 40 mg/kg of TQ, respectively, before 0.5 h of ischemia, and then 3 h of ovarian ischemia was applied; (6) and (7) 3-hour ovarian ischemia was applied; 2.5 h after the induction of ischemia, rats were administered the same doses of TQ; at the end of 3 h of ischemia, a 3-hour reperfusion was applied. Histologic changes under light microscopy, immunoreactivity for anticaspase-3 and serum levels of malondialdehyde, interleukin-6, catalase and glutathione peroxidase were noted and compared between the 7 groups. Results: Ischemia and ischemia/reperfusion cause a deterioration of biochemical and histopathological parameters. Administration of TQ seems to reverse these alterations and alleviate the injury. Antioxidant defense mechanisms appear to be enhanced by the administration of TQ. Conclusion: TQ at different doses attenuates ovarian ischemia and ischemia/reperfusion injury in rats.

Protective effects of thymoquinone against cholestatic oxidative stress and hepatic damage after biliary obstruction in rats

The aim of this study was to examine the preventive and therapeutic effects of thymoquinone (TQ) against cholestatic oxidative stress and liver damage in common bile duct ligated rats. A total of 24 male Sprague-Dawley rats were divided into three groups: control, bile duct ligation (BDL) and BDL + received TQ; each group contain 8 animals. The rats in TQ treated groups were given TQ (50 mg/kg body weight) once a day orally for 2 weeks starting 3 days prior to BDL operation. To date, no more biochemical and histopathological changes on common bile duct ligated rats by TQ treatment have been reported. The application of BDL clearly increased the tissue hydroxyproline (HP) content, malondialdehyde (MDA) levels and decreased the antioxidant enzyme [superoxide dismutase (SOD), glutathione peroxidase (GPx)] activities. TQ treatment significantly decreased the elevated tissue HP content, and MDA levels and raised the reduced of SOD, and GPx enzymes in the tissues. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with TQ attenuated alterations in liver histology. The immunopositivity of alpha smooth muscle actin and proliferating cell nuclear antigen in BDL were observed to be reduced with the TQ treatment. The present study demonstrates that oral administration of TQ in bile duct ligated rats maintained antioxidant defenses and reduces liver oxidative damage and ductular proliferation. This effect of TQ may be useful in the preservation of liver function in cholestasis.