This study evaluated the impact of various drugs on cognitive function and oxidative stress in a chronic insomnia rat model induced by rapid eye movement (REM) sleep deprivation using modified multiple-platform method. Forty-eight albino rats were divided into eight groups (n=6 per group): the control group; REM sleep-deprived groups, which were treated with water, corn oil, donepezil, vinpocetine, Coenzyme Q10 + corn oil, ramipril, and Coenzyme Q10 + corn oil + ramipril. Spatial learning and memory were assessed using the Morris water maze. On the 3rd and 4th days of the acquisition trials, the latency of Coenzyme Q10, ramipril and their combination was lower than that of REM sleep-deprived rats. In the probe trial, sleep-deprived rats spent significantly less time in the target quadrant than REM controls . In contrast, vinpocetine, Coenzyme Q10 and the combination of ramipril + Coenzyme Q10 resulted in a significantly greater percentage of time spent in the target quadrant than REM sleep-deprived rats . Biochemical analysis of hippocampal tissue revealed that, compared with REM sleep-deprived rats, those treated with donepezil, vinpocetine, ramipril, Coenzyme Q10, or their combination presented reduced malondialdehyde and acetylcholinesterase levels but increased reduced glutathione levels. In conclusion, these findings suggest that donepezil, vinpocetine, ramipril, Coenzyme Q10, and their combination effectively ameliorate the cognitive deficits and oxidative stress induced by REM sleep deprivation.
Gram-negative bacteria's outer membranes include lipopolysaccharides (LPS), which are a major contributor to inflammatory eye disorders. LPS cause apoptosis induction and produce reactive free radicals of oxygen (ROS). In microglia, LPS-induced ROS stimulates transient receptor melastatin 2 (TRPM2), whereas glutathione (GSH) and N-(p-amylcinnamoyl) anthranilic acid (ACA) decrease their activation. Anti-apoptotic and antioxidant properties of GSH through TRPM2 inhibition were not reported in human retinal pigment epithelial (ARPE-19) cells. Therefore, the modulator action of GSH on the TRPM2-mediated molecular oxidant and apoptotic pathways in ARPE-19 was investigated. Five main groups were generated in the ARPE-19: Control, GSH (10 mM for 2 h), LPS (1 μg/ml for 24 h), LPS + GSH, and LPS + ACA (25 μM for 30 min). The amounts of ROS, mitochondrial dysfunction, apoptosis, caspases (caspase-3, -8, and -9), and cytosolic free Ca2+ were increased by the LPS incubation, while the incubations of GSH and ACA reduced their amounts. The viable cell number and viability percentage were decreased by LPS, but their viability and number were increased by the incubations of GSH and ACA. In conclusion, GSH decreased the levels of LPS caused oxidative stress and apoptosis via suppressing TRPM2 in the ARPE-19. One possible treatment agent for oxidative retinal injury and inflammatory eye diseases induced by LPS could be the GSH treatment.
The growing interest in foods that can be beneficial to human health has recently gained global attention. People have used pumpkin seed oil in cooking and traditional medicine since ancient times. Recent data indicated that it is used also in the pharmaceutical industry. So, this study was undertaken to evaluate the protective effect of pumpkin seed oil against oxidative damage in diabetic rats fed a low-zinc diet. Animals were equally divided into five groups: three groups were fed a sufficient-zinc diet, one non-diabetic group, and two groups diabetic rats, one untreated group and the other treated with a 5% pumpkin seed oil diet. The remaining two groups were diabetics fed a zinc-deficient diet, one non-treated and the other treated with 5% pumpkin seed oil diet. After four weeks of the treatments, fasting rats were sacrificed. Zinc deficiency led to decreased body weight (p
The trace element selenium (Se) has anti-apoptotic and antioxidant properties. When stimulated by lipopolysaccharide (LPS), brain and neural cells undergo apoptosis and produce reactive oxygen species (ROS). LPS-induced ROS stimulates transient receptor potential melastatin 7 (TRPM7) activation, whereas carvacrol (CRV) and Se inhibit it. The mechanisms by which Se inhibits LPS-induced oxidative stress and apoptosis in neuronal (SH-SY5Y) cells remain unknown. To protect SH-SY5Y cells from ROS-induced apoptosis and death, I investigated how Se alters the TRPM7-mediated molecular pathways. Five main groups were generated in the SH-SY5Y:Control, Se (1 μM for 2 hours), LPS (1 μg/ml for 24 hours), LPS + Se, and LPS + TRPM7 blocker (CRV). Apoptosis, ROS, mitochondrial dysfunction, apoptotic markers (caspase-3, -8, and -9), and cytosolic free Ca2+ were increased by the LPS incubation, whereas Se and CRV treatments reduced these parameters. The LPS decreased cell viability; however, the viability in the LPS + Se and LPS + CRV groups increased with the incubations of Se and CRV.In conclusion, Se decreased LPS-induced oxidative stress and apoptosis by inhibiting TRPM7 in the neuronal cells. One possible treatment agent for oxidative neuronal injury and neurodegenerative disorders induced by LPS could be the Se treatment.
Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive, behavioural, and personality declines. In the etiology of AD, oxidative stress has a main role. This study was carried out to investigate the neuroprotective effects of vitamins C and E on cognitive function and oxidative stress in rats with scopolamine-induced AD. After seven days of treatment with vitamins C and E, AD was induced in the rats on day eight by the injection of 4 mg/kg body weight of scopolamine. Behavioural outcomes such as anxiety, learning and memory were carried out using an elevated plus-maze, and novel object recognition tasks. Malondialdehyde (MDA), antioxidant enzymes, and vitamins were assessed in the brain tissue. Vitamins C and E treatment enhanced memory and behavioural functions in dementia rats when compared with the control group. The results also showed that the vitamin C and vitamin E treated groups had higher brain levels of vitamin C and vitamin E compared to the control group. Furthermore, both treatments reduced the MDA levels compared to the control group. The group that received either of the vitamins indicated higher superoxide dismutase and catalase activities compared to the control group. In conclusion, the results suggest that both vitamins exhibited neuroprotective properties by ameliorating oxidative stress and improving cognitive outcomes in dementia rats.
The role of 8-hydroxydeoxyguanosine (8-OHdG) as a biomarker in breast cancer remains controversial with conflicting results across studies. This case-control study aimed at comparing serum 8-OHdG levels between breast cancer patients and healthy controls, and examine associations with clinical characteristics. Thus, 71 Iraqi women (47 newly diagnosed, treatment-naïve breast cancer patients and 24 controls) were used from November 2024 to June 2025. Demographic data and lifestyle factors were collected through structured questionnaires. No significant difference was found in median 8-OHdG levels between breast cancer patients and controls. No correlations were observed between 8-OHdG and age, BMI, tumor grade, or hormone receptor status. Our findings suggest that 8-OHdG may not serve as a general screening biomarker for breast cancer, as its levels were comparable across all clinical and pathological parameters examined.
This study aimed to compare demographic, embryological, and biochemical parameters between male factor infertility and unexplained infertility groups undergoing IVF treatment. Demographic parameters such as age and BMI, along with embryological factors including the number of oocytes retrieved, MII oocytes, fertilization rate, and Grade II embryo quality, were evaluated. Biochemical markers, including MDA, GSH, GSH-Px, vitamin A, vitamin E, and ß-carotene, were also analyzed. No significant differences were observed between the two groups regarding demographic or embryological outcomes (p > 0.05), although Grade I embryo quality showed a significant difference (p = 0.047), underscoring the importance of embryo quality in IVF success. The clinical pregnancy and live birth rates were higher in the control group, but the differences were not statistically significant. Further biochemical analysis revealed significantly higher MDA levels in the patient group, indicating increased oxidative stress (p < 0.001). Conversely, antioxidant levels, including GSH, GSH-Px, vitamin A, and vitamin E, were found to be lower in the patient group, suggesting a weakened defense against oxidative stress. These results highlight the critical role of oxidative stress and antioxidant status in IVF outcomes. Specifically, increased MDA levels and decreased antioxidant activity were linked to lower oocyte and embryo quality. Despite these findings, no significant differences were noted in pregnancy, clinical pregnancy, and birth rates between the groups. In conclusion, this study emphasizes the importance of managing oxidative stress through antioxidant levels to potentially improve IVF success rates. Future research should further explore the biochemical parameters influencing IVF outcomes to refine treatment strategies for different infertility causes.
Chemotherapy drugs such as carboplatin are commonly used to treat various cancers, including testicular, lung, and ovarian cancer. Although carboplatin primarily targets cancer cells, it can also damage healthy cells, including neurons, leading to potential adverse effects. Notably, some side effects of carboplatin therapy are associated with nerve cells and the nervous system. The aim of our study was to investigate the potential protective effects of chrysin (Chr) against carboplatin-induced toxicity in SH-SY5Y neuronal cells. In this study, the ameliorative effects of Chr on carboplatin-induced cellular toxicity were evaluated through cell viability assays, lipid peroxidation (LPO) analysis to assess antioxidant capacity, TUNEL assay, immunohistochemistry (IHC) staining, and western blotting to examine anti-apoptotic activities. The results indicated that Chr mitigates carboplatin toxicity in SH-SY5Y cells by reducing LPO levels and the expression of cytochrome c (Cyt c) and Bax, while increasing the expression of the anti-apoptotic protein Bcl-2. The study also demonstrated that carboplatin caused apoptosis by causing DNA strand breaks while Chr treatment alleviated these effects. These findings suggest that the use of antioxidants, particularly Chr, may diminish the apoptotic effects of carboplatin in SH-SY5Y cells and could provide insights into potential therapeutic strategies for mitigating cell damage caused by carboplatin.
Although the pathology and clinical symptoms of Parkinson's disease (PD) are well-defined, the cellular and molecular mechanisms underlying the selective degeneration of dopaminergic neurons remain unclear. Mitochondrial dysfunction and neuroinflammation are increasingly recognized as central contributors to the pathogenesis of PD. The leaf extract of Ginkgolide, Ginkgo biloba, is known for its neuroprotective properties in several neurodegenerative diseases. In the present study, we sought to investigate the neuroprotective mechanism of Ginkgolide B (BN52021), a terpene lactone derived from the leaf of Ginkgo biloba, in an animal model of PD. Adult C57BL/6 mice treated with MPTP (30 mg/ kg b.wt.) exhibited significant motor deficits, ameliorated by cotreatment with BN52021 (20 mg/ Kg b.wt.), as evidenced by improved motor behaviors. MPTP administration resulted in a marked reduction in the mitochondrial complex I activity and antioxidant enzymes, specifically in the substantia nigra, whereas the striatum remained unaffected. Notably, BN52021 cotreatment restored the complex I function and antioxidant enzymes in the substantia nigra, highlighting its region-specific neuroprotective properties. Additionally, MPTP exposure significantly increased myeloperoxidase activity, a marker of oxidative stress and inflammation mitigated by BN52021. Moreover, the inflammatory markers NLRP3, MCP-1, and IL-1β were significantly upregulated following MPTP administration, indicating the activation of the inflammasome pathway. However, coadministration of MPTP with BN52021 effectively suppressed the upregulation of these inflammatory markers, suggesting a strong anti-inflammatory effect. These findings underscore the therapeutic potential of Ginkgolide in PD, primarily through its ability to enhance mitochondrial electron transport complex I activity, restore antioxidant defense, and suppress neuroinflammation.
Common and vision-threatening inflammatory ocular disorders are major issues on a global scale. The etiology and whole treatment for inflammatory disorders are yet unknown. With the exception of human retinal pigment epithelial-19 (ARPE-19), numerous cells have been shown to be involved in lipopolysaccharide (LPS)-induced free reactive oxygen species (ROS) and apoptosis through TRPV1 cation channel stimulation. I wanted to determine how TRPV1 affected the oxidative cytotoxicity and apoptosis caused by LPS in ARPE-19. Two main groups in the ARPE-19 cells were induced as control and LPS (1 g/ml for twenty-four hours). TRPV1 antagonist (100 M capsazepine (CAPZ) for 1 hour) blocked TRPV1 in the channel, whereas TRPV1 agonist (10 M capsaicin (CAPS) for 1 hour) stimulated cells of the main groups. The incubation of CAPS increased the amounts of apoptosis, caspases (caspase -3, -8, and -9), mitochondrial dysfunction, and ROS in the control and LPS groups, while CAPZ incubation diminished these amounts. However, their amounts were additionally increased in the LPS than in the control. LPS-induced increases of cell viability were diminished in the control and LPS groups by the CAPZ. In summary, CAPZ treatment through TRPV1 inhibition contributes to the oxidative stress and apoptosis that LPS causes in ARPE-19 cells. TRPV1 inhibition by CAPZ may be a viable treatment option for oxidative retinal damage induced by LPS.
The transformation of our era, resulting in a change in dietary habits towards a higher intake of fatty foods, presents a worldwide health issue. Among these challenges is neurodegeneration, which leads to cognitive impairment. It is imperative to seek alternative solutions rooted in nature to address the limitations associated with non-natural treatment methods. This entails harnessing the properties of secondary metabolite compounds found in plants, such as Colocasia esculenta Var. Mentawai. This research aims to assess the efficacy of C. esculenta Var. Mentawai corm as neuroprotective agents in mitigating CNS damage and preventing cognitive decline associated with neurodegeneration. Daily administration of a high-fat diet and a mixture of taro flour is conducted on young adult male mice for a duration of 60 days. Furthermore, analysis of the neurocognitive ability of mice, determination of malondialdehyde levels, and observation of histopathological structures on brain tissue were carried out. The results showed that the group of mice fed with taro flour mixture effectively showed a positive impact on maintaining neurocognitive abilities and histopathological structure of brain tissue against neurodegeneration (p
Age impairs cognitive functions and antioxidant defenses, for example, by increasing oxidative stress and inflammation in the brain. However, so far, there is no report on the consequences of aging on temporal patterns of proteins and lipids oxidation, antioxidant enzymes activity, endogenous clock and proinflammatory cytokine, in the prefrontal cortex (PFC). Therefore, our objectives here were: 1) to investigate the endogenous nature of 24h-rhythms of lipoperoxidation, protein carbonyls levels, CAT and GPx activity, RORa, and TNFα, in the rat PFC, and 2) to study the consequences of aging on the circadian organization of those factors in the same brain area. To do that, 3- and 22-mo-old male Holtzman rats were maintained under constant darkness conditions during 15 days before reaching the corresponding age. PFC samples were isolated every 4 h, under dim-red light, during a 24h period. Our results revealed circadian patterns of antioxidant enzymes activity, oxidative stress, RORa and TNFα proteins levels, in the PFC of young rats. The circadian distribution of the rhythms’ phases suggests the existence of a reciprocal communication among the antioxidant defenses, the endogenous clock, and the inflammation, in the PFC. Noteworthy, such circadian organization disappears in the PFC of aged rats. An increased oxidative stress would make the redox environment to change into an oxidative status, which alters the endogenous clock activity and disrupts the circadian organization of, at least part, of the antioxidant defenses and the TNFα, in the PFC. These results might highlight novel chronobiological targets for the design of therapeutic strategies addressed to a healthy aging.
Sevoflurane is an anesthetic, and it acts on oxidative activity by activating Ca2+ influx. In human neutrophils, oxidative stress activates the voltage-gated calcium channels (VGCC) and the TRPM2 channel; on the other hand, these channels are inhibited by 2-aminoethoxydiphenyl borate (2-APB) and verapamil plus diltiazem (V+D), respectively. Under sevoflurane anesthesia, surgical arthroscopy poses a significant risk to oxidative stress and Ca2+ influx-induced neutrophil infiltration and injury of patients. However, vitamin E may inhibit lipid peroxidation (LP) by upregulating reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) but downregulating TRPM2 and VGCC in the neutrophils of surgical arthroscopy patients. This topic was examined in the current study. We enrolled 20 patients in the current study, separating them into two primary groups: patients and patients plus vitamin E. Ten patients were divided into two groups: preoperative (N1) and postoperative (N2), both of which were not given vitamin E therapy. The remaining ten patients were given 300 IU of vitamin E two hours prior to their surgical arthroscopy (E1), and their blood was again drawn following the procedure (E2). Prior to fMLP stimulation, the isolated neutrophils from each of the four groups were cultured with 10 uM V+D and 100 uM 2-APB. In the neutrophils, there was an increase in intracellular free Ca2+ ([Ca2+]i) concentration and LP levels due to the downregulation of GSH and GSH-Px; however, following vitamin E treatment, GSH concertation and GSH-Px activity increased in the E2 group. While 2-APB and V+D treatment reduced the concentration of [Ca2+]i in the neutrophils, vitamin E administration had no effect on this measurement. In summary, vitamin E treatment mitigated the GSH and GSH-Px alterations induced by I/R damage, while TRPM2 and VGCC inhibition reduced the [Ca2+]i rise induced by I/R injury. One potential treatment approach for I/R-induced oxidative neutrophil damage is the suppression of TRPM2 and VGCC.
Drug-resistant epilepsy, a commonly devastating condition, affects more than 50 million people globally. Type 2 diabetes mellitus (T2DM) is associated with an increased risk of neurological disorders, and a potential association between epilepsy and subsequent T2DM has emerged. Inhibiting sodium-glucose linked transporters (SGLTs), which are differentially expressed in the brain, has been shown to reduce epileptic episode activity. This study aimed to evaluate the anticonvulsive effect of empagliflozin in rats with seizures induced by maximal electric shock (MES) and pentylenetetrazol (PTZ). Generalized tonic‒clonic seizures were induced in the rats using an electroconvulsive meter, and pentylenetetrazol was injected to induce absence seizures. The duration of all the stages of seizure and Racine stage scoring (RSS) were performed. Malondialdehyde (MDA), nitric oxide (NO) and reduced glutathione (GSH) levels in the brain tissues were determined. Histopathological analysis of the brain tissues was carried out. A significant (p <0.01) decrease in the duration of tonic hind limb extension (THLE), a significant decrease in the levels of pro-oxidants such as MDA and NO, and an increase in the levels of antioxidants such as GSH were observed in the low dose 10 mg/kg and high dose 20 mg/kg empagliflozin groups compared to the disease control group. Histopathological analysis revealed a greater number of healthy neurons with few dark-stained cells in the treatment groups, suggesting the neuroprotective effect of empagliflozin. The present study showed that empagliflozin modulates epileptic activity. Empagliflozin has a potential role in the management of epilepsy in diabetic patients.
One bioactive element of honeybee venom is melittin (MEL). MEL induced oxidant and apoptotic activities through the increase of mitochondrial Zn2+ and Ca2+ in tumor cells, but it also induced neuroprotective activity by inhibiting the cell death, intracellular reactive oxygen species (iROS), and mitochondrial ROS (mROS) productions in neurons. By stimulating the TRPM2 channel, hypoxia (HPO) enhances the effects of oxidative stress and neuronal death; however, its inhibition prevents the alterations. I studied the neuroprotective effect of MEL on HPO-mediated oxidative neurotoxicity and cell death in SH-SY5Y neuronal cells by altering the TRPM2 signaling pathways. In the SH-SY5Y cells, five groups were induced as control, MEL (1 ug/ml for 24 hrs), HPO (CoCl2 and 200 M for 24 hrs), HPO + MEL, and HPO + TRPM2 antagonist (2-aminoethoxydiphenyl borate, 2APB) (100 M for 2 hrs). The amounts of cytosolic free Ca2+ were increased in the HPO group by the stimulation of hydrogen peroxide, although they were decreased in the cells by the treatment of 2APB and MEL. The amount of cytosolic free Ca2+ was higher in the HPO group than in the control group. The amounts of cell death (propidium iodide positive cell number), oxidants (mROS and iROS), mitochondrial membrane depolarization, and cytosolic free Zn2+ were higher in the HPO group than in the control and MEL groups, although their amounts were lower in the HPO + MEL and HPO + 2APB groups than in the HPO group only. In conclusion, MEL therapy reduced the amount of HPO-induced oxidative stress and neuronal deaths in SH-SY5Y cells by inhibiting TRPM2. The MEL could be considered as a potential protective component against oxidative neuronal damage caused by HPO.
Rapid and uncontrollable cell proliferation, altered metabolism, and abnormal vasculature of cancer cells make them hypoxic and result in the generation of reactive oxygen species (ROS), causing oxidative stress. Hypoxia-mediated oxidative stress represents a significant barrier to effective cancer treatment. miRNAs are emerging as a potential regulator of hypoxia-responsive genes and hypoxia-mediated oxidative stress. Based on the role of miR-140-5p in regulating a hypoxia-responsive gene, this study is aimed at understanding the miR-140-5p role in regulating hypoxia-mediated oxidative stress under breast tumor hypoxia. We found that the miR-140-5p might control the hypoxia-mediated ROS generation by regulating the Nrf2 expression. Knowing the significance of miR-140-5p in regulating hypoxia-mediated oxidative stress and breast tumor progression, targeting miR-140-5p might represent a promising strategy for anti-breast cancer therapy.
Ferroptosis is a non-apoptotic cell death closely related to a metabolic pathway involving iron overload, imbalanced glutathione metabolism, oxidative stress and lipid peroxidation damage. Obesity is closely associated with these imbalances. In this study, we aimed to investigate the effect of hippocampal ferroptosis in an obesity model and the potential role of N-acetylcysteine (NAC) against ferroptosis. A high-fat (60%) dietary pattern was used to establish an obesity model for 15 weeks. NAC was administered to NAC and Obese+NAC (ObNAC) groups by oral gavage at a dose of 150 mg/kg for 3 weeks. Glutathione peroxidase 4 (GPX4) and the cystine transporter solute carrier family 7- member 11 (SLC7A11) expression levels were investigated immunohistochemically to detect ferroptosis in hippocampal tissues. In the statistical analysis, H-scores of GPX4 and SLC7A11 in the hippocampus sections of the Ob group were significantly lower than in the control, NAC and ObNAC groups (p
Migraine is a complex neurological problem whose primary symptom is headache and is common in the human population. It is well known that neuroinflammation plays a vital role in the pathogenesis of migraine, with adverse effects on the nervous system, including headache disorders such as migraine. The infusion of the nitric oxide donor glyceryl trinitrate (GTN) is often used in experimental models of migraine because it is the best-known model of migraine provocation. N-(p-amyl cinnamoyl) anthranilic acid (ACA) has been shown to inhibit both TRPM2 and phospholipase A2 (PLA2). Recent research has explored potential interventions to mitigate GTN-induced neurotoxicity. One such candidate is ACA, a compound with anti-inflammatory and antioxidant properties. Thirty-six C57BL/6j black mice were divided into the control groups of ACA, GTN, and ACA+GTN. Mice in the ACA were treated intraperitoneally with ACA (25 mg/kg) for three days. Mice in the GTN were treated intraperitoneally with a single dose of GTN (10 mg/kg) for migraine induction. After the experimental stages were completed, the mice in all groups were sacrificed, and brain tissue and erythrocyte samples were taken from the mice. The levels of inflammatory cytokines (TNF α, IL 1β, and IL 6), apoptosis, intracellular ROS, lipid peroxidation, caspase 3-9, and mitochondrial membrane potential increased in the GTN group. However, their levels were decreased in the ACA+GTN group by the injection of ACA. The treatment of ACA regulated the GTN treatment-induced decreases of glutathione levels, glutathione peroxidase activation, and cell viability in the brain and erythrocytes. In conclusion, GTN plays a role in neurotoxicity caused by increased apoptosis and ROS. We observed that ACA modulated the brain and erythrocyte oxidant, antioxidant parameters, and apoptotic processes. The neuro-protective role of ACA treatment may be explained by its modulating activity against increased apoptosis and oxidative stress.
Classic non-homeostatic structures involved in food intake regulation are reciprocally influenced by metabolic signals. Orexigenic peptides expressed in the olfactory bulb (OB) and hippocampus (HP) modulate olfactory processing and memory, respectively. Hypothalamic circuits also modulate feeding behavior by activating and releasing Agouti-related peptide (AgRP) in response to orexigenic signals. An adequate response to fasting requires the expression of p75 neurotrophin receptor (p75NTR) in AgRP neurons. The present study aimed to determine whether there is a role for p75NTR and AgRP in the OB and HP on the feeding behavior of fasted rats. A group of fasted rats (FG) was confronted with a decision-making paradigm in a T-maze containing a standard chow pellet (CP), and the same pellet coated with a phenolic-rich avocado paste extract (AVO) on either end; their OB and HP were then analyzed with histological and molecular tools. FG rats had briefer feeding latencies, as compared to control rats fed ad libitum (median latencies: 55.4 vs 191.7 min, p = 0.032). They also had reduced cell counts in both brain structures, as compared to satiated rats. AgRP mRNA was not expressed in the HP of either group, however, it was found in the OB. p75NTR mRNA was expressed in both brain structures of FG rats. These results suggest that contrasting metabolic states (fasted or satiated) motivate different feeding responses, which are influenced by p75NTR and AgRP mRNA expression in non-homeostatic food intake brain structures.
Diabetes, which causes oxidative stress-induced neuronal damage, is still one of the most important chronic health problems in the world. It can cause serious cellular loss and damage throughout the course of the disease. It is hypothesized that increased oxidative stress in this process increases free reactive oxygen species (ROS) and apoptotic markers and causes diabetic damage. Alpha-Lipoic acid (α-LA), which has a direct antioxidant effect in ROS reduction reactions, is also among the main components of the antioxidant system that works for free radical control and apoptosis. To understand the role of α-LA in reducing diabetes-induced oxidative damage, we examined the production of ROS in the brain cortex and erythrocytes of rats and their effects on markers of apoptosis. Forty adult Wistar albino rats were divided into four groups as control, α-LA, diabetic (DIA), and DIA+α-LA. For the induction of diabetes, the intraperitoneal injection of a dose of streptozotocin (STZ) (45 mg/kg) was used. α-LA (50 mg/kg) was applied to the groups of α-LA and DIA+α-LA for 14 days. At the end of the experiment, the brain cortex tissue and erythrocyte samples were taken from the rats. The levels of apoptosis, caspase 3, caspase 9, mitochondrial membrane potential, intracellular ROS, and lipid peroxidation were increased in the STZ group, although their levels were decreased in the DIA+α-LA group by the injection of α-LA. The STZ treatmentinduced decreases of cell viability, reduced glutathione, and glutathione peroxidase were increased in the brain and erythrocytes by the treatment of α-LA. In conclusion, diabetes acted a role in neuronal damage caused by increased ROS and apoptosis. We observed that α-LA induced a modulatory role on the apoptotic, oxidant, and antioxidant parameters in the brain and erythrocyte. The neuroprotective role of α-LA treatment may be explained by its modulating activity against increased oxidative stress and apoptosis.
