جستجوی مقالات مرتبط با کلیدواژه « Oxidative stress » در نشریات گروه « پزشکی »

In this study, we aimed to investigate the protective effect of Thymoquinone (THQ) against testicular damage caused by Methotrexate (MTX).

This study consists of 5 groups: Control, Olive oil, THQ, MTX, and MTX+THQ. At the end of the experiment, spermiogram analysis was performed on the rats. In addition, testicular tissues were taken and histopathology, immunohistochemistry, and biochemistry analysis were performed. Biochemical analyses were performed on the serums.

According to the results obtained, spermiogram values, Johnson’s testicular biopsy score, SOD, CAT, GPx, FSH, LH, and testosterone values were statistically significantly decreased in the MTX group compared to the control group. In the MTX+THQ group, spermiogram values, Johnson’s testicular biopsy score, SOD, CAT, GPx, FSH, LH, and testosterone values increased statistically significantly compared to the MTX group. NRF2 and HO-1 immunoreactivity were statistically significantly decreased in the MTX group compared to the control group. In the MTX+THQ group, NRF2 and HO-1 immunoreactivity were statistically significantly increased compared to the MTX group. The level of MDA, which is important in lipid damage, and the level of biochemistry results of TNF-α, IL1-β, and IL-6, which are important markers, and the results of p-NF-kB and P38 immunoreactivity were statistically significantly increased in the MTX group compared to the control group. In the MTX+THQ group, these parameters showed a significant decrease compared to the MTX group.

According to these results, it is thought that THQ will play a protective role against infertility caused by chemotherapy-induced testicular damage.

Neurodegenerative diseases and brain tumors are significant medical ailments that impact the brain. Administering therapeutic drugs to the brain is more challenging compared to other organs or systems. The existence of the blood-brain barrier (BBB) poses significant complexities and challenges in delivering drugs to the brain. This study explores the potential of Fullerene nanoparticles as a novel therapeutic agent for delivering drugs to the brain and their neuroprotective roles within the central nervous system. Novel drug delivery methods have been devised to surmount obstacles posed by BBB and accomplish targeted drug delivery to the brain. Carbon nanostructures are an excellent option for delivering drugs into the brain because they have favorable biocompatibility and can easily penetrate BBB. Furthermore, these nanocarriers has the potential to serve as a therapeutic agent inside the central nervous system, exhibiting neurogenerative properties in some cases. Additionally, their impact on the proliferation of neurons and their ability to counteract the formation of amyloid plaques is particularly remarkable. Carbon-based nanomaterials, including zero-dimensional fullerene (C60), one-dimensional carbon nanotubes (CNTs), and two-dimensional graphene, have shown significant potential in the area of nanomedicine. This is attributed to their unique blend of chemical and physical characteristics, as well as their hydrophobic surfaces. Fullerene nanoparticles have the potential to greatly improve the treatment of brain illnesses by serving as both carriers and therapeutic agents.

Chronic alcohol abuse causes cognitive deficits. Huangqi Gegen Decoction (HGD), a traditional Chinese herbal formula comprising Huangqi and Gegen, has been documented for its therapeutic efficacy in the treatment of alcoholic liver injury. However, its potential neuroprotective effects against alcohol-induced brain injury remain unexplored. This study aims to evaluate the neuroprotection of HGD on alcohol-induced cognitive dysfunction and the associated mechanism.

Wistar rats were orally administered 50% ethanol for 10 weeks, followed by treatment with HGD at doses of 16, 32, or 64 mg/kg/day for an additional 6 weeks. The spatial learning and memory abilities of rats were assessed through the Morris Water Maze experiment. The pathological condition in the hippocampus was assessed using H&E and Nissl staining. Tight junction proteins, oxidative stress, and inflammation cytokines were measured by IF, ELISA, PCR, and western blot. The mRNA and protein expression of Keap1, Nrf-2, HO-1, and NQO-1 were tested by PCR and western blot.

Results showed that HGD effectively mitigated cognitive dysfunction and pathological changes in alcohol-induced rats while enhancing the expression of ZO-1, Occludin, and Claudin-5. Furthermore, HGD effectively mitigated oxidative stress by reducing levels of ROS and MDA, while elevating levels of SOD, CAT, and GSH-PX in brain tissue. Moreover, HGD significantly suppressed microglial activation and down-regulated expressions of IL-1β, IL-6, and TNF-α. Mechanistically, HGD remarkably up-regulated the expression of Nrf-2, HO-1, and NQO-1 while down-regulating Keap1 expression.

These findings suggest that HGD may be a promising therapeutic agent for alleviating alcohol-induced cognitive dysfunction.

Diabetic nephropathy is one of the main causes of kidney failure in the end stage of diabetes worldwide. The present study was conducted with the aim of using the remote ischemic conditioning (RIC) method to prevent diabetic nephropathy.

Diabetes was induced by high-fat diet (60%) and streptozotocin injection (35 mg/kg) in rats. RIC was performed by tightening a tourniquet around the upper thigh and releasing it for three cycles of 5 min of ischemia and 5 min of reperfusion daily for an 8-week duration. At the end of the experiment, serum and urine parameters were examined. Anti-oxidant enzymes and lipid peroxidation levels in the kidney were also determined along with histological examination. The expression levels of tumor necrosis factor-alpha and transforming growth factor beta genes were also evaluated. 

Glucose, cholesterol, triglyceride, and HbA1c concentrations were not significantly reduced in the RIC group. On the other hand, serum creatinine, urea, and albumin levels decreased and increased in urine. Anti-oxidant enzymes did improve in the kidney significantly and the expression of tumor necrosis factor-alpha and transforming growth factor beta genes decreased significantly. Histopathological examination also showed that necrosis, epithelial damage, and leukocyte infiltration increased in the diabetic group and improved in the treatment group. 

The results of biochemical analysis, and enzymatic and histological examinations showed that although RIC could not reduce blood glucose and lipids, nevertheless it may delay the progression of diabetic nephropathy due to the presence of anti-inflammatory and anti-oxidant activities.

This study was conducted to explore the impact of 1, 8-cineole (eucalyptol) on the biochemical, molecular, and histological changes caused by lead acetate in the liver of adult male Wistar rats. The research also investigated the potential involvement of the TLR4 signaling pathway in this effect. 

Rats were orally administered lead acetate (25 mg/kg-day) for 14 consecutive days and received 1, 8-cineole (100 mg/kg-day) during the same period. 

1, 8-cineole prevented an increase in the malondialdehyde level, a decrease in the glutathione level, and a decrease in the activity of superoxide dismutase and glutathione peroxidase enzymes in the liver of rats treated with lead acetate. This monoterpene also prevented an increase in the expression of pro-inflammatory cytokines and significantly reduced the infiltration of inflammatory cells in the liver parenchyma. Additionally, 1, 8-cineole discouraged the increase in toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa B (NF-κB) expression in the liver and stopped a rise in serum AST and ALT enzymes. 

1, 8-cineole can prevent liver damage caused by lead acetate by reducing oxidative stress and inflammation. This hepatoprotection is probably achieved by inhibiting TLR4/MyD88/NF-κB signaling.

Garlic, scientifically known as Allium sativum, has been a revered traditional medicine for millennia, rich in diverse phytochemicals with various medicinal properties, such as antioxidant, anticancer, anti-inflammatory, pain killer, hypoglycemic, antimicrobial, antiviral, and wound-healing properties. Its remarkable therapeutic potential makes garlic a beneficial natural treatment for many health issues.

This research examined the neuroprotective effects of garlic against Malathion (Mal)-associated Parkinson's-like behavioral symptoms in rats.

Animals were categorized into eight groups at random: (1) saline-treated group (control); (2) Mal group (100 mg kg⁻¹); (3) Mal + garlic (50 mg kg⁻¹); (4) Mal + garlic (100 mg kg⁻¹); (5) Mal + garlic (150 mg kg⁻¹); (6) Mal + L-DOPA (10 mg kg⁻¹); (7) garlic (150 mg kg⁻¹); and (8) polyethylene glycol (PEG) group (L-DOPA vehicle). Treatment lasted 28 days, followed by behavioral assessments and analyses of acetylcholinesterase (AChE) activity, malondialdehyde (MDA) level, antioxidants levels, and proinflammatory cytokines in the striatum.

Mal exposure caused neurobehavioral toxicity with increased MDA, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), alongside decreased GSH concentration and AChE activity. Garlic treatment successfully mitigated these effects.

The findings suggest that garlic may have a favorable impact in treating Parkinson's disease by enhancing antioxidant levels and mitigating oxidative stress and inflammatory processes, countering the harmful effects of pesticides like Mal. Additional studies necessary to thoroughly explore garlic's protective benefits in this area.

The kidneys are the main target of lead toxicity as lead is accumulated in and excreted through the kidneys. The main lead toxicity occurs through oxidative stress and lipid peroxidation, causing cellular damage in the kidneys. Moringa leaves contain high levels of flavonoids, with antioxidant effects that are useful in treating diseases accompanied by oxidative stress due to toxicity. Our goal was to analyze the attenuation effects of Moringa leaves extract on lead-induced nephrotoxicity in male Wistar rats.

This research was conducted based on an experimental design and post-tests. Forty-eight Wistar rats were randomly divided into four groups as follows: control group (K), which was given lead acetate at 750 mg/kg/day for 7 days, and three other groups of P1, P2 and P3, which were given lead acetate at the same dose for 7 days followed by administering with the ethanolic extract of Moringa leaves at 1,000, 1,500, and 2,000 mg/kg/day doses orally for 14 days, respectively.

There were improvements in oxidative stress in the kidneys of the study rats, marked by an increase in the serum levels of GSH, GPx, CAT, and SOD, and a decrease in the kidney MDA levels. Kidney disorders can be improved by administering ethanol extract from Moringa leaves, which is characterized by a significant decrease in blood BUN and creatinine levels.

All doses of the ethanolic extract of Moringa leaves reduced the oxidative stress and improved the kidney function impaired due to acute exposure to lead in male Wistar rats.

Cancer occurs in 83% of liver diseases. Other risk factors for liver cancer include viral hepatitis, alcohol consumption, industrial chemicals, and a number of toxins. Another major disease that occurs following liver damage is hepatic encephalopathy. This condition arises primarily due to increased blood ammonia levels. Carvacrol, with antioxidant properties, reduces oxidative stress on the liver. The aim of this study was to investigate the effect of carvacrol on the improvement of hepatic encephalopathy in rats.

In this experimental study, 60 male Wistar rats were randomly divided into six groups of 10 each. Liver damage and induction of oxidative stress were caused in the rats by administering thioacetamide (100 mg/kg/day) intraperitoneally for three consecutive days. Carvacrol was administered by gavage at 25, 50, or 100 mg/kg/day after thioacetamide treatment. We investigated the biomarkers of liver damage in the blood, such as alanine transaminase, lactate dehydrogenase, total protein, and bilirubin. We also assessed the effect of oxidative stress, as the key inducer of hepatic encephalopathy, on the liver by measuring the lipid peroxidation, antioxidants, reactive oxygen species, glutathione reserves, and ammonium levels in the serum and brain.

Thioacetamide significantly increased the biochemical markers in the rat sera, reflecting ammonium release and the development of oxidative stress (P<0.05). Conversely, the various doses of carvacrol significantly reduced the levels of biomarkers that are indicative of liver damage (P<0.05).

The study findings provided experimental evidence in favor of the therapeutic effects of carvacrol and against liver injury induced by thioacetamide, leading to encephalopathy.

Methadone is a substance widely used in the substitution treatment of opiate addiction in pregnancy. The placental transfer of methadone influences oxidative stress processes. Melatonin is a hormone with antioxidant activity.

This study aimed to evaluate the protective effects of melatonin on oxidative stress induced by the transfer of transplacental methadone in mice.

In this experimental study, 36 female mice (2 months old, 20 ± 2 gr) were divided into 6 groups (n = 6/each) of control, methadone (0.3 mg/kg intraperitoneal, single dose) and melatonin (2, 4, and 6 mg/kg/day gavage) were administered 30 min before methadone, and one group received melatonin alone (0.6 mg/kg with single injection). Administration for 10 consecutive days of the pregnancy period was done. After baby mice were born, all neonatal mice were killed by beheading or sacrificing after anesthesia. The liver tissues were extracted. The samples were then sent for studying oxidative stress markers such as lipid peroxidation, glutathione, and protein carbonyl contents. Also, we have used the immunohistochemistry method for apoptotic markers such as: BAX, Bcl2, and Caspase3 for assaying apoptosis.

This study has shown that methadone caused a significant decrease in glutathione concentration (p = 0.035). Also, we observed a significant increase in lipid peroxidation and protein carbonyl contents (p = 0.015, 0.025 respectively). However, melatonin treatment significantly inhibited oxidative stress markers (p = 0.025). Also, apoptosis assay has shown that melatonin could decrease BAX and Caspase 9 as apoptotic and increase Bcl2 as an antiapoptotic proteins (p = 0.015).

Our findings have shown that melatonin has a protective effect against oxidative stress and apoptosis induced by the placental transfer of methadone via its antioxidant effects.

In this study, the protective effects of native Iranian probiotics (Lactobacillus rhamnosus, Lactobacillus casei and Lactobacillus holoticus) on lead acetate (PbAc)-induced toxicity in the kidney of male rats were investigated using biochemical, molecular and histopathological approaches. Twenty-one male Wistar rats were divided into three groups (n=7/group), including controls, PbAc recipient (10 mg/kg) and PbAc recipient (10 mg/kg) + probiotic mixture (109 CFU). PbAc and probiotics were gavage in the groups. On the 31st day, blood samples were used to measure serum concentrations of creatinine (Cr), blood urea nitrogen (BUN), sodium, total protein and potassium. Rats were dissected and renal tissues apoptotic and inflammatory genes were evaluated. PbAc increased serum concentrations of Cr, sodium, and urea, and decreased total protein and potassium, while it enhanced interleukine-6 (IL-6) and tumor necrosis factor -α (TNF- α) gene expression in kidney tissue compared to the control group.  Probiotic mixture decreased Cr, BUN, and malondialdehyde and increased activity of catalase and superoxide dismutase enzymes in kidney tissue. The results of the study showed that the native Iranian probiotics mixture can be used to protect the function and structure of the kidneys against toxic and oxidative damage induced by PbAc.

Hashimoto's thyroiditis (HT) is one of the common causes of hypothyroidism. Although various factors are involved in its development, recently the role of oxidative stress in its pathogenesis has been known. The present study aimed to investigate the level of total antioxidant capacity (TAC), catalase (CAT), and salivary superoxide dismutase (SOD) in patients with HT compared with the control group. The present case-control design included patients aged 18-80 years suffering from HT referred to the endocrine clinic. Eligible patients were selected by the available sampling method. Complete unstimulated saliva was collected under a rest state in a comfortable room between 10:00 AM and 12:00 AM and a checklist was used to collect data. The chi-square, t-test, and Mann-Whitney U tests were used for data analysis using SPSS 22 software. The mean age of the participants was 36.55±9.37 years (range: 20-56). The two groups were the same in terms of age and gender (P>0.05). The findings indicated that the difference in the means CAT between the two groups was 22.63 which was strongly and statistically significant (P<0.001). In this study, the level of TAC and SOD in Hashimoto's thyroid patients was decreased and the level of CAT was increased. These initial findings show that oxidative stress can be associated with Hashimoto's thyroid disease or the possibility of developing this disease increase.

 Evidence declared lipopolysaccharide (LPS) initiates inflammatory responses by stimulating the abandon of cytokines, which may perturb organ function. On the other side, it has been suggested Cedrol has potential properties, including anti-inflammatory and anti-oxidative activities. Herein, this study was done to assess the protective effect of Cedrol against LPS-associated heart damage.

 Thirty-five rats (200-250 g) were sorted into five groups, including control, LPS, LPS-Cedrol 7.5 mg/kg, LPS-Cedrol 15 mg/kg, and LPS-Cedrol 30 mg/kg groups. Cedrol was administrated through injected intra-peritoneally for two weeks. The heart tissues were removed and malondialdehyde (MDA) as a lipid peroxidation marker, superoxide dismutase (SOD), and catalase (CAT) as antioxidant markers were assessed. Furthermore, the interleukin (IL)-6 level in cardiac tissue was measured and Masson’s trichrome methods were employed to appraise cardiac inflammation and fibrosis, respectively.

 Inflammation induced by LPS was significantly accompanied by myocardial fibrosis which was shown by Masson’s trichrome staining (P<0.001). In addition, LPS administration enhanced the MDA level while it diminished the activity of anti-oxidant markers such as CAT and SOD (P<0.001 for all cases). In the histological results, Cedrol improved LPS-induced inflammation and cardiac fibrosis (P<0.01 to P<0.001). Cedrol also enhanced CAT and SOD activities, whereas declined MDA level in the cardiac tissue (P<0.01 to P<0.001).

 The current findings proposed that the administration of Cedrol exerted a protective role in LPS-associated heart damage by reducing inflammation, cardiac fibrosis, and oxidative stress.

Diabetes is the most common metabolic disease, associated with hyperglycemia and long-term complications. This study aimed to elucidate the anti-diabetic role of oleuropein (OLE) in a streptozotocin (STZ)-induced diabetic animal model.

Adult male Wistar rats (200–250 g) were randomly divided into four groups: 1) Control group, 2) STZ group: diabetic rats that received STZ (60 mg/kg), 3) OLE 50 group: diabetic rats treated with oral OLE at 50 mg/kg of body weight daily for 28 days, and 4) OLE 100 group: diabetic rats treated with oral OLE at 100 mg/kg of body weight daily for 28 days. Memory function and biochemical factors such as malondialdehyde (MDA) levels, glutathione peroxidase (GPx), and total thiol activity were evaluated in the rats' cerebral cortex and striatum tissues. Moreover, nuclear transcription factor-kappa B (NF-κB) and nuclear factor E2-related factor 2 (Nrf2) pathway activation were determined in cerebral cortex and striatum tissues by real-time polymerase chain reaction (PCR).

Chronic administration of OLE ameliorated cognitive deficits and attenuated oxidative stress induced by diabetes. Additionally, OLE significantly prevented the activation of the pro-inflammatory marker NF-κB and downregulated Nrf2 expression in STZ-induced diabetic rats.

Our results confirm the significant protective role of OLE against STZ-induced diabetes in rats by up-regulating Nrf2 signaling and enhancing antioxidant activity.

Studies indicate that phytoestrogens and phytosterols have adverse effects on the male reproductive system. To our knowledge, the effects of Tanacetum parthenium on testicular tissue, spermatozoa chromatin integrity and free radical damage have not yet been investigated. Therefore, this study aimed to evaluate the effect of T. parthenium administration on sperm parameters, testis histology, sperm DNA integrity and oxidative damage in adult male mice. 

Eighteen adult male mice (2-3 months old) were randomly divided into 3 groups: control, TP1 and TP2. TP1 and TP2 groups were separately gavaged with 50 and 100 mg/kg T. parthenium. After harvesting the epididymis, sperm analysis was performed according to the guidelines of the World Health Organization (WHO). The testicular tissue also passaged through the tissue routine process after being placed in a formalin fixative solution. To check the quality of sperm chromatin, a sperm smear was prepared and then stained with acridine orange dye and was examined with a fluorescent microscope. Biochemical parameters, including malondialdehyde (MDA), thiol, catalase enzyme, and superoxide dismutase (SOD), were measured in testicular tissue. Finally, data were analyzed by the analysis of variance in SPSS software, version 16. 

A significant reduction was seen in sperm count and sperm morphology percentage and the germinal epithelium thickness in the TP1 and TP2 groups versus the control group. The spermatozoa with DNA damage in percentage were higher in the TP1 group (21.22±3.70) and TP2 group (42.60±3.73) compared to the control group (2.40±4.3). There were remarkable differences between the three groups in MDA (P≤0.001) and thiol (P≤0.001) levels. Catalase level (P≤0.001) was lower in the TP1 and TP2 groups than in the control group. 

The results of this study showed that T. parthenium caused a significant decrease in sperm chromatin quality, MDA level and germinal epithelium thickness at both doses. A reduction was found in the antioxidant enzyme level in the mice administrated with 50 and 100 mg/kg of T. parthenium.

This study aims to comprehensively assess the therapeutic potential of clove extract in mitigating testicular damage and preserving male reproductive function under hypoxic conditions in male rats.

We randomly divided 24 male rats into three groups: a hypoxia group that just received normal saline, a hypoxia + clove extract (4 mg/kg) group, and a sham operation group without treatment. After eight weeks, the serum level of oxidative stress parameters was examined, and the testicle histopathological examination, such as seminiferous tubule diameters and epithelium thickness, was assessed.

The serum malondialdehyde (MDA) concentration was significantly enhanced in the hypoxic group, and the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx) declined (P<0.05). The diameters and thickness of the seminiferous tubule were diminished notably (P<0.05). Johnson’s score decreased in the hypoxic group. Treatment with clove extract also led to improvements in this parameter.

Our study provides compelling evidence for the therapeutic potential of clove extract in mitigating testicular injury associated with varicocele-induced testicular hypoxia in male rats.

This study aimed to investigate the potential protective impact of anthocyanin against tissue damage and oxidative stress provoked by varicocele within the testes of adult rats.

A total of 32 male rats were divided into four groups as follows: a control group undergoing a sham procedure, a varicocele group without intervention (V), a varicocele group treated with anthocyanin (VA), and a group receiving anthocyanin treatment alone. Following a 56-day treatment period, the indicators of oxidative stress were gauged in the blood plasma, while histological modifications were evaluated utilizing the hematoxylin and eosin staining technique.

In the varicocele group treated with anthocyanin, we observed noteworthy enhancements in Johnsen score, epithelium thickness, and seminiferous tubule diameter compared to the untreated varicocele group. Treatment groups exhibited substantial elevations in testosterone levels and antioxidant enzyme levels. Furthermore, there was a reduction in the levels of malondialdehyde (MDA), an established marker of oxidative damage, and a decline in histological damage in the treatment groups.

The outcomes underscore the potential safeguarding influence of anthocyanin against testicular damage stemming from varicocele induction, suggesting its beneficial role in countering oxidative stress and tissue impairment.