Protective Effect Of L-carnitine Research Articles

The protective effects of L-Carnitine against oxidative toxicity in adult male New Zealand Rabbits

The protective effects of L-Carnitine against oxidative toxicity in adult male New Zealand Rabbits

Protective effects of L-carnitine against beta-amyloid-induced memory impairment and anxiety-like behavior in a rat model of Alzheimer's disease

Alzheimer's disease (AD), the most common cause of dementia, leads to neurodegeneration and cognitive decline. We investigated the therapeutic effects of L-carnitine on cognitive performance and anxiety-like behavior in a rat model of AD induced by unilateral intracerebroventricular injection of β-amyloid1-42 (Aβ1-42). L-carnitine (100 mg/kg/day) was administered intraperitoneally for 28 consecutive days. Following this, the open-field test, novel object recognition test, elevated plus-maze test, Barnes maze test, and passive avoidance learning test were used to assess locomotor activity, recognition memory, anxiety-like behavior, spatial memory, and passive avoidance memory, respectively. Plasma and hippocampal oxidative stress markers, including total oxidant status (TOS) and total antioxidant capacity (TAC), were examined. In addition, histological investigations were performed in the dentate gyrus of the hippocampus using Congo red staining and hematoxylin and eosin staining. The injection of Aβ1-42 resulted in cognitive deficits and increased anxiety-like behavior. These changes were associated with an imbalance of oxidants and antioxidants in plasma and the hippocampus. Also, neuronal death and Aβ plaque accumulation were increased in the hippocampal dentate gyrus region. However, injection of L-carnitine improved recognition memory, spatial memory, and passive avoidance memory in AD rats. These findings provide evidence that L-carnitine may alleviate anxiety-like behavior and cognitive deficits induced by Aβ1-42 through modulating oxidative-antioxidant status and preventing Aβ plaque accumulation and neuronal death.

L-carnitine co-administration prevents colistin-induced mitochondrial permeability transition and reduces the risk of acute kidney injury in mice

Colistin is a polymyxin antibiotic currently experiencing renewed clinical interest due to its efficacy in the treatment of multidrug resistant (MDR) bacterial infections. The frequent onset of acute dose-dependent kidney injury, with the potential of leading to long-term renal damage, has limited its use and hampered adequate dosing regimens, increasing the risk of suboptimal plasma concentrations during treatment. The mechanism of colistin-induced renal toxicity has been postulated to stem from mitochondrial damage, yet there is no direct evidence of colistin acting as a mitochondrial toxin. The aim of this study was to evaluate whether colistin can directly induce mitochondrial toxicity and, if so, uncover the underlying molecular mechanism. We found that colistin leads to a rapid permeability transition of mitochondria isolated from mouse kidney that was fully prevented by co-incubation of the mitochondria with desensitizers of the mitochondrial transition pore cyclosporin A or L-carnitine. The protective effect of L-carnitine was confirmed in experiments in primary cultured mouse tubular cells. Consistently, the relative risk of colistin-induced kidney damage, calculated based on histological analysis as well as by the early marker of tubular kidney injury, Kim-1, was halved under co-administration with L-carnitine in vivo. Notably, L-carnitine neither affected the pharmacokinetics of colistin nor its antimicrobial activity against relevant bacterial strains. In conclusion, colistin targets the mitochondria and induces permeability transition thereof. L-carnitine prevents colistin-induced permeability transition in vitro. Moreover, L-carnitine co-administration confers partial nephroprotection in mice treated with colistin, without interfering with its pharmacokinetics and antibacterial activity.

Protective effects of l-carnitine on isoprenaline -induced heart and kidney dysfunctions: Modulation of inflammation and oxidative stress-related gene expression in rats

The aim of this study was to evaluate the effect of l-carnitine (L-CAR) treatment on isoprenaline (ISO) administered kidney and heart impairment in male Long Evans rats. Four groups of rats were engaged in this study such as control, ISO, control + L-CAR, and ISO + L-CAR, where n = 6 in each group. The rats were also provided with chow food and water ad libitum. At the end of the study, all rats were sacrificed, and blood and tissue samples were collected for bio-chemical analysis. Oxidative stress parameters and antioxidant enzyme activities were determined in plasma and tissues. Antioxidant and inflammatory genes expression were analyzed in the kidney cortex, and histopathological studies of kidney tissues were performed. This study showed that creatinine and uric acid in plasma were significantly increased in ISO-administered rats. l-carnitine treatment lowered the uric acid and creatinine level. ISO-administered rats showed increased lipid peroxidation and declined levels of antioxidant enzymes activities in kidneys and heart. l-carnitine treatment restored antioxidant enzymes activities and protect against oxidative stress in kidney and heart. This effect is correlated with the restoration of Nrf-2-HO-1 genes expression followed by increased SOD and catalase genes expression in the kidney. l-carnitine treatment also prevented the TNF-α, IL-6, and NF-кB expression in kidneys of ISO administered rats. Histopathology staining showed that l-carnitine treatment prevented kidney damage and collagen deposition in ISO administered rats. The result of this study exhibited that l-carnitine treatment reduced oxidative stress and increased antioxidant enzyme activities by enhancing antioxidant genes expression in ISO administered rats.

L-carnitine fails to rescue chemotherapy injured ovaries by epigenetic changes of transcription factors

Cyclophosphamide (CP), as an anti-cancer drug, is frequently used to treat various types of cancer. A decreased number of ovarian follicles impaired normal ovarian function, and subsequent premature ovarian failure (POF) presented as a side effect of cyclophosphamide usage. These events may eventually affect the fertility rate of individuals. The present study showed the effect of cyclophosphamide on ovarian reserves and the protective effect of L-carnitine (LC) as an antioxidant to prevent POF.To design the study, six to eight-week-old NMRI female mice were divided into three groups: control, cyclophosphamide (CP), and cyclophosphamide + L-carnitine (CP + LC). Mice received drugs intraperitoneally (IP) for 21 days. In the following 24 h after the last injection, both ovaries were used to evaluate the expression of Sohlh1 and Lhx8 genes by Real-time PCR. Furthermore, the alteration of Lhx8 promoter methylation was examined by Methylation-sensitive high-resolution melting analysis (MS-HRM).The present data showed the negative effect of CP on regulator genes of oogenesis including Sohlh1 and Lhx8. In addition, an examination of the epigenetic status of the Lhx8 gene showed a change in promoter methylation of this gene following cyclophosphamide injection. Although, L-carnitine is an effective antioxidant in relieving oxidative stress caused by cyclophosphamide and its damage, in the present study, however, the use of L-carnitine failed to protect the ovaries from changes caused by CP injection. So, using cyclophosphamide can alter the expression of folliculogenesis genes through its effects on epigenetic changes and may cause POF. The results of the present study showed that L-carnitine consumption can’t protect the ovaries against the adverse effects of CP.

Protective Effect of L-Carnitine against Deltamethrin Induced Male Reproductive Toxicity in Adult Rats Exposed at their Prepubertal Stage

The present study aims to investigate the protective role of L-Carnitine (LC) against Deltamethrin-induced testicular toxicity in male rats exposed during their early developmental period. DTM was administered at a dose of 6 mg/kg body weight to the prepubertal rat’s Post-Natal Day (PND) 23 rats through oral route and exposure was continued until they reach PND 90. After completion of the exposure period, male rats were assessed for reproductive endpoints. Deltamethrin exposure caused a significant reduction in testosterone production and decreased the sperm parameters such as sperm count, sperm motility, sperm viability and sperm membrane integrity. Deltamethrin intoxication also reduced the reproductive organs’ weight and testicular steroidogenic enzymes (3β-hydroxysteriod dehydrogenase and 17β-hydroxysteriod dehydrogenase) levels. Further DTM exposure induced the oxidative stress as evidenced by the significant reduction in the superoxide dismutase, catalase, and glutathione levels with significant elevation in the malondialdehyde. DTM also induced the significant sperm DNA damage. In addition, DTM exposure significantly declined the testosterone levels over the control group, indicating the impaired steroidogenesis. In addition to the compromised steroidogenesis DTM exposure also deteriorated the testicular architecture according to the histological observations. On the other hand, therapy with LC (100 mg/kg body weight) improved the biomass of reproductive organs, the features of the sperm, testicular steroidogenesis and testicular antioxidant enzymes levels. Concluding that DTM might disturb the testicular antioxidant level that eventually impaired the reproductive health of rats. However, LC supplementation mitigated the reproductive toxicity through its antioxidant property.

Protective effect of L-carnitine against ethanol-induced gastric damage: investigation of possible mechanisms of action

The underlying mechanisms of L-carnitine’s (L-CAR) protective effect against ethanol (EtOH)-induced gastric mucosal damage were investigated in this study. The rats were randomly divided into four groups: control (CON), EtOH, EtOH + L-CAR50, and EtOH + LCAR100. Control group was given saline (5 mL/kg) twice at 1-hour interval. EtOH group was given 5 mL/kg saline 1-hour before absolute EtOH administration (5 mL/kg). EtOH + LCAR50 group received 50 mg/kg LCAR 1-hour before absolute EtOH administration (5 mL/kg). EtOH + LCAR100 group received 100 mg/kg LCAR 1-hour before absolute EtOH administration (5 mL/kg). All the rats were euthanized 1 hour after the administration of EtOH. The gastric lesion area was grossly examined, and gastric lesions were histopathologically evaluated. Real-time PCR was used to examine the expression of cyclooxygenase 1 and 2 (COX-1 and COX-2), inducible- and endothelial- nitric oxide synthase (iNOS and eNOS), tumor necrosis factor alpha (TNF-α), heat shock protein 70 (HSP70), and trefoil factor 2 (TFF2) mRNA in the gastric mucosa. Histopathological examination revealed that L-CAR treatment reduced the severity and extent of gastric lesions caused by EtOH administration, such as shedding of the superficial epithelium, glandular gland necrosis, intralesional hemorrhage, submucosal edema, and neutrophil infiltration. L-CAR administration was found to significantly reduce the mRNA levels of COX-2, iNOS, eNOS, and TNF-α in the gastric mucosa compared to EtOH administration alone. It was determined that L-CAR administration further increased the gastric mucosal HSP70 mRNA expression than EtOH administration alone. L-CAR treatment increased TFF2 expression which was decreased after EtOH administration. Finally, L-CAR administration was thought to protect against EtOH-induced gastric mucosal damage by regulating the expression of gastric mucosal COX and NOS systems, reducing the inflammatory cytokine levels, inducing a cellular stress response, and stimulating the expression of factors associated with mucus secretion and gastric epithelium restitution.

Evaluation of L-Carnitine Potential in Improvement of Male Fertility.

L-carnitine, through its antioxidant potential, plays a significant role in reducing ROS production in male genital tract; therefore, fundamental improvements in spermatogenesis process and sperm structural and functional parameters in seminal plasma can be observed by treatment with L-carnitine. A literature search was performed using PubMed (including Medline) from the database earliest inception to 2021. Eligibility criteria included studies on protective effects of L-carnitine against damages to the male reproductive system. Based on the findings of the current study, L-carnitine has an effective potential to protect testis and improve conventional and functional sperm parameters against ROS-induced damages by sperm cryopreservation, busulfan treatment, and radiation.

Protective Effects of L-carnitine and Co-enzyme Q10 Against Oxidative Stress Damage in Hypertension

In this study, it was aimed to investigate the effects of L-carnitine and Co-enzyme Q10 administration together with ACE Inhibitor (ACE inh.) on oxidative stress parameters in liver, brain and kidney tissues in L-NAME hypertensive rats. At the study, divided all rats into eight groups, four groups with 14 days of experiment time and four groups with 28 days of experiment time. At the end of the experiment, the rats were euthanized and their liver, brain and kidney tissues were taken. Malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) activities were measured in tissue supernatants. While NO and MDA levels increased in all tissues, a significant decrease was observed in GSH levels (P<0.001). In conclusion, it is suggested that supplementation of L-carnitine and CoQ10 can be considered as a combination therapy strategy for patients prone to higher levels of oxidative stress and inflammation.

Protective Effects of L-carnitine and Co-enzyme Q10 Against Oxidative Stress Damage in Hypertension

In this study, it was aimed to investigate the effects of L-carnitine and Co-enzyme Q10 administration together with ACE Inhibitor (ACE inh.) on oxidative stress parameters in liver, brain and kidney tissues in L-NAME hypertensive rats. At the study, divided all rats into eight groups, four groups with 14 days of experiment time and four groups with 28 days of experiment time. At the end of the experiment, the rats were euthanized and their liver, brain and kidney tissues were taken. Malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) activities were measured in tissue supernatants. While NO and MDA levels increased in all tissues, a significant decrease was observed in GSH levels (P

Protective effects of L-carnitine on X irradiation-induced uterus injury via antioxidant and anti-inflammatory pathways

Purpose Ionizing radiation causes oxidative stress induced tissue damage as well as a decline in reproduction incidence. The purpose of our study was to evaluate the effects of L-carnitine on radiation-induced uterine injury. Materials and methods Thirty Wistar albino rats were classified into five groups. Physiological saline was administered intraperitoneally to the control group. A single dose of 8.3 Gy whole body X-irradiation was applied to the radiation-1 and radiation-2 groups. These groups were sacrificed on the 6th hour and 4th day, respectively, after irradiation. Radiation-1 + L-carnitine and radiation-2 + L-carnitine groups received a daily dose of 200 mg/kg L-carnitine in addition to the same dose of irradiation. L-carnitine was also applied one day before and four days after irradiation. Results L-carnitine therapy partially blocks the depletion of the deep glands and radiation-induced flattening of the glandular epithelium and endometrial surface. Proinflammatory cytokines such as IL-1β, IL-6 and TNF-α were found to be significantly expressed in the uterus tissue of irradiated mice. In the radiation groups, NFκB and PARP-1 expressions in uterine tissue was significantly increased compared to L-carnitine treated and the control groups. It was observed that the oxidative stress index increased in the radiation groups, but decreased in the L-carnitine applied groups. Conclusions Our findings showed that L-carnitine has a positive effect on radiation-induced uterine damage. L-carnitine may be a potential safe radio protective agent during radiotherapy for pelvic cancer provided the tumor is not protected from radiation damage to the same extent as the normal tissue is. However, prospective clinical trial studies are necessary to understand its efficacy.

Assessment of L-carnitine effectiveness on carpal tunnel syndrome.

Background: Carpal tunnel syndrome (CTS) is the most prevalent entrapment neuropathy. Due to the results of recent studies about the protective effects of L-carnitine on nerves, this study was conducted to evaluate the effects L-carnitine on CTS improvement in terms of patient's function, electrodiagnostic study (EDX), and median nerve sonography. Methods: In this double-blind, randomized, controlled trial, patients with CTS were selected based on the inclusion and exclusion criteria, and then, divided into two groups of placebo and L-carnitine at a dose of 500 mg twice daily for 6 weeks. They were assessed at baseline, and 4 and 6 weeks later using Boston Carpal Tunnel Questionnaire (BCTQ)‎, median nerve conduction study (EDX), and sonography. Results: There was no statistically significant difference between the intervention and control groups in terms of BCTQ‎ scores, electrodiagnostic findings, and sonographic indexes. Although based on the results of the repeated measures test of the intervention and control groups separately, there was a statistically significant difference in some electrodiagnostic criteria and BCTQ‎ scores. These indexes improved after the intervention. Conclusion: The effectiveness of L-carnitine on mild to moderate CTS improvement cannot be approve based on the findings of this study and more studies and systematic reviews are required in this regard.

The protective effect of L-carnitine on testosterone synthesis pathway, and spermatogenesis in monosodium glutamate-induced rats

BackgroundMonosodium glutamate (MSG) is a food ingredient that is increasingly used commercially. MSG leads to oxidative stress, consequently suppressing steroid hormone production that causes defects in male reproductive system. This study aimed to evaluate the effect of L-carnitine as an antioxidant on testicular damage in MSG-induced male rats.MethodsSixty adult male Spargue-Dawley rats were randomly divided into six groups of ten as follows: control (water), sham (normal saline), L-carnitine (200 mg/kg b.w), MSG (3 g/kg b.w), MSG + L-carnitine 100 (3 g/kg b.w of MSG and 100 mg/kg b.w of L-carnitine), and MSG + L-carnitine 200 (3 g/kg b.w of MSG and 200 mg/kg b.w of L-carnitine). The treatment was administered by oral gavage for six months. Serum levels of Malondialdehyde (MDA), Total Anti-oxidant Capacity (TAC), LH, FSH, testosterone, and mRNA expressions of Star, Cyp11a1, and Hsd17b3 genes, and histological and stereological changes were assessed.ResultsL-carnitine led to a significant decrease in the level of MDA and a significant rise in the serum levels of TAC, LH, FSH, and mRNA expression of Star and Cyp11a1 compared to the MSG group (p < 0.05). Furthermore, stereological results indicated a significant increment in the number of sexual lineage cells, the total volume of the testis, length, diameter, and volume of seminiferous tubules, the height of the germinal epithelium, sperm count, and sperm motility (p < 0.05) in MSG + L-carnitine 200 compare to MSG group.ConclusionThe study’s findings demonstrated that L-carnitine due to its anti-oxidant properties, ameliorated the reproductive abnormalities in the male rats exposed to MSG.

L-carnitine Attenuates DNA Damage and Oxidative Stress in Diabetic Animals

Background: Diabetes is a metabolic disorder characterized by high plasma glucose levels. In this disease, increased production of reactive oxygen species (ROS) results in DNA damage and multiple complications. L-carnitine (LC) has shown a potent antioxidant activity that may reduce oxidative stress. Objectives: This study aims at assaying the effect of LC on DNA damage in streptozotocin-induced diabetic rats and evaluating the changes in antioxidant markers and liver function enzymes after the administration of LC . Methods: In the present study, for induction of diabetes, we injected a single dose of streptozotocin (65 mg/kg) by the intraperitoneal route, and diabetic rats were treated with LC 200, 300, and 400 mg/kg daily for 3 weeks. We detected the DNA damage at 7, 14, and 21 days after induction diabetes by the comet assay method. The blood glucose level, plasma alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were tested. Also, we measured the activity levels of superoxide dismutase (SOD) and intracellular glutathione (GSH). Results: The results of this study demonstrated the increasing amount of DNA damage with the amount and duration of hyperglycemia. L-carnitine treatment significantly decreased the parameters of genotoxicity such as % DNA in the tail, tail length, and tail moment over time. Moreover, the treatment of diabetic rats with LC 300 and 400 mg/kg/day after 21 days led to a remarkable decrease in blood glucose than diabetic rats. Also, we observed that LC can ameliorate enzyme liver function and reduce oxidative stress via enhancement of GSH and SOD levels. Conclusions: The results of this study indicated the protective effect of LC against DNA damage and oxidative stress in diabetic rats.

Protective effect of l-carnitine on oxidative stress in the liver of acute hepatotoxicity male ratsafter cytarabine chemotherapy

Hepatotoxicity is a common clinical manifestation associated with a wide range of anticancer therapies. Because of the inherent toxicity of anticancer therapies, oncologists must maintain a broad understanding of their effects on the body, including the liver.Therefore, the study was conducted to examine the effects of two doses of L-carnitine on damaged liver as a result of giving cytarabine. Twenty-four male rat were used in the experiment. The rats divided to four group each group with six rats,the first group injected normal salineintraperitoneally and set as control group(G1),the second group injected cytarabine 25 mg/kg/bw intraperitoneally and set as (G2), the third injected cytarabine 25 mg/kg/bw and 50 mg /kg/bw L-carnitine intraperitoneally and set as (G3), the third injected cytarabine 25 mg/kg/bw and 300mg/kg/bw L-carnitine Intraperitoneally and set as(G4), the study showed that use of L-carnitine reduced the harmful effect of cytarabinein the body when compared to the group that was injected only with cytarabineat level of (p-value &lt;0.05). ALT show a significant increase in G2 when compared to other groups the mean value was (104±7.697, 134.66±13.08, 105.66±5.89, 94.33±3.5) for groups: control, cytarabine,50mg/kg/bw &amp; 300mg/kg/bw ofL-carnitine respectively;,,

Comparative Study between Protective Effects of L-Carnitine and Curcumin on Nephrotoxicity Induced by Cisplatin in Adult Male Albino Rats

Comparative Study between Protective Effects of L-Carnitine and Curcumin on Nephrotoxicity Induced by Cisplatin in Adult Male Albino Rats

Protective effect of L-carnitine on myocardium after PCI in patients with acute ST segment elevation myocardial infarction.

article: Protective effect of L-carnitine on myocardium after PCI in patients with acute ST segment elevation myocardial infarction - Minerva Medica 2023 February;114(1):112-5 - Minerva Medica - Journals

Protective effects of L-carnitine on behavioral alterations and neuroinflammation in striatum of glutaryl-COA dehydrogenase deficient mice

Glutaric acidemia type 1 (GA1) is caused by glutaryl-CoA dehydrogenase deficiency that leads to a blockage in the metabolic route of the amino acids lysine and tryptophan and subsequent accumulation of glutaric acid (GA), 3-hydroxyglutaric acids and glutarylcarnitine (C5DC). Patients predominantly manifest neurological symptoms, associated with acute striatal degeneration, as well as progressive cortical and striatum injury whose pathogenesis is not yet fully established. Current treatment includes protein/lysine restriction and l-carnitine supplementation of (L-car). The aim of this work was to evaluate behavior parameters and pro-inflammatory factors (cytokines IL-1β, TNF-α and cathepsin-D levels), as well as the anti-inflammatory cytokine IL10 in striatum of knockout mice (Gcdh−/-) and wild type (WT) mice submitted to a normal or a high Lys diet. The potential protective effects of L-car treatment on these parameters were also evaluated. Gcdh−/- mice showed behavioral changes, including lower motor activity (decreased number of crossings) and exploratory activity (reduced number of rearings). Also, Gcdh−/- mice had significantly higher concentrations of glutarylcarnitine (C5DC) in blood and cathepsin-D (CATD), interleukin IL-1β and tumor factor necrosis alpha (TNF-α) in striatum than WT mice. Noteworthy, L-car treatment prevented most behavioral alterations, normalized CATD levels and attenuated IL-1β levels in striatum of Gcdh−/- mice. Finally, IL-1β was positively correlated with CATD and C5DC levels and L-car was negatively correlated with CATD. Our results demonstrate behavioral changes and a pro-inflammatory status in striatum of the animal model of GA1 and, most importantly, L-car showed important protective effects on these alterations.

The Comparison of the Protective Effect of L-Carnitine, Chromium and Vitamin D with Metformin on Liver, Antioxidant Enzyme Activity, and Iron Metabolism in Diabetic Rats

Objective: Due to the lack of information about the positive or negative effects of L-carnitine, chromium, vitamin D, and the uptake of a safe dietary supplement to reduce the effects of diabetes, it seems essential to determine the effects of these drugs on diabetes. Materials and Methods: Wistar rats were divided into 12 groups, control, diabetic, and intact, each of which was treated with metformin, L-carnitine, vitamin D, and chromium or a combination of L-carnitine, vitamin D, and chromium. The serum levels of liver function parameters, iron, TIBC, Catalase and GPX activities were measured. Data were statistically analyzed by one-way ANOVA using SPSS 18 software. Statistical significance among the groups was determined using LSD test, and P-value&lt; 0.05 was considered significant in all cases. Results: AST activity in diabetic groups and those receiving chromium and L-carnitine has significantly reduced (P-value= 0.009). A significant reduction in ALT and ALP activity in the diabetic groups receiving vitamin D and combined and non-diabetic groups receiving metformin were observed, in contrast to a significant increase in ALT activity in diabetic recipients of Lcarnitine (P-value= 0.009). Conclusion: L-carnitine, chromium, and vitamin D supplements have synergistic effects and a combination of them has the best protective effect on factors that have been studied.

Effect of L-carnitine and atorvastatin on a rat model of ischemia-reperfusion injury of spinal cord

ABSTRACT Pro-inflammatory cytokines and reactive oxygen species (ROS) are produced in acute spinal cord injury, leading to myelin breakdown, inflammation, mitochondrial dysfunction, and apoptosis of neurons and glial cells. The aim of the present study was to investigate possible protective effects of L-carnitine (carn) or atorvastatin (ator) on spinal cord ischemia-reperfusion injury (IRI). Rats were randomized into nine equal groups (n = 8): control and control taking carn (100 mg/kg BW), ator (2.5 mg/kg BW) or both, as well as sham-operation, IRI and IRI taking same doses of carn, ator or both. Neurological assessments were done 48 hours after IRI, and serum nitrite/nitrate was measured. Finally, lumbar segments of spinal cord were excised, and part was homogenized and prepared for measuring tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), malondialdehyde (MDA), advanced oxidation protein products (AOPP), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase. The other part was sectioned for evaluation of histopathological changes and for immunostaining by glial fibrillary acidic protein (GFAP), Bax and Bcl-2. The IRI increased ROS (nitrite/nitrate, MDA, AOPP) and pro-inflammatory cytokines (TNF-α, IL-1β), and decreased antioxidants (GSH, GPx, SOD, catalase) with impaired sensory and motor functions. Astrogliosis was detected by GFAP, and increased apoptosis was demonstrated by increasing Bax and decreasing Bcl-2. Treatment with carn or ator alone decreased TNF-α, IL-1β, nitrite/nitrate, MDA and AOPP, and increased GSH, GPx, SOD, and catalase with improvement of neurological functions and histological studies. Combination of carn and ator improved most of measured IRI-affected parameters better than isolated carn or ator administration.