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The present study was conducted to investigate the effects of Ocimum basilicum L. (OB) extract on learning and memory impairment in aged rats. Male rats were divided into the following experimental groups: Group 1 (control): including 2 months old rats, Group 2 (aged) including 2 years old rats, Groups 3–5 (aged-OB): including 2 years old rats received 50, 100, and 150 mg/kg OB for 8 weeks by oral gavage. Aging increased the delay to find the platform but, however, decreased the time spent in the target quadrant when tested by Morris water maze (MWM). Aging also reduced the latency to enter the dark chamber in the passive avoidance (PA) test compared to the control group. Moreover, interleukin-6 (IL-6) and malondialdehyde (MDA) levels were raised in the hippocampus and cortex of aged rats. In contrast, thiol levels and enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) significantly reduced. In addition, aging significantly reduced BDNF expression. Finally, OB administration reversed the mentioned effects. The current research showed that OB administration improves learning/memory impairment induced by aging. It also found that this plant extract protects the brain tissues from oxidative damage and neuroinflammation. [ABSTRACT FROM AUTHOR]

Background: Tolerance to the analgesic effects of opioids and non-steroidal anti-inflammatory drugs (NSAIDs) is a major concern for relieving pain. Thus, it is highly valuable to find new pharmacological strategies for prolonged therapeutic procedures. Biguanide-type drugs such as metformin (MET) are effective for neuroprotection and can be beneficial for addressing opioid tolerance in the treatment of chronic pain. It has been proposed that analgesic tolerance to NSAIDs is mediated by the endogenous opioid system. According to the cross-tolerance between NSAIDs, especially sodium salicylate (SS), and opiates, especially morphine, the objective of this study was to investigate whether MET administration can reduce tolerance to the anti-nociceptive effects of SS. Methods: Fifty-six male Wistar rats were used in this research (weight 200-250 g). For induction of tolerance, SS (300 mg/kg) was injected intraperitoneally for 7 days. During the examination period, animals received MET at doses of 50, 75, or 100 mg/kg for 7 days to evaluate the development of tolerance to the analgesic effect of SS. The hot plate test was used to evaluate the drugs' anti-nociceptive properties. Results: Salicylate injection significantly increased hot plate latency as compared to the control group, but the total analgesic effect of co-treatment with SS + Met50 was stronger than the SS group. Furthermore, the effect of this combination undergoes less analgesic tolerance over time. Conclusions: It can be concluded that MET can reduce the analgesic tolerance that is induced by repeated intraperitoneal injections of SS in Wister rats. [ABSTRACT FROM AUTHOR]

Introduction: 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. Methods: 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. Results: 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). Conclusion: 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. [ABSTRACT FROM AUTHOR]

Background The present study aimed to assess the efficacy of folic acid (FA) on withdrawal following nicotine (Nic) administration in adolescent male rats. Aims and Methods Adolescent male rats were divided into two groups: (1) vehicle and (2) Nic (Nic-2 mg/kg), and were under treatment from 21 to 42 days of age. After that, they continued the experiment without treatment and returned to a regular diet, except for one of those who received Nic. The rats were divided into four groups where they were treated with different doses of FA (5, 10, and 15 mg/kg) and bupropion (Bup) by oral gavage, and the final group included normal rats that received only FA (15 mg/kg) from 42 days of age for three weeks during which withdrawal occurred. Results Results showed that adolescent Nic exposure exacerbated the behavioral indices of anxiety- and depression-like behaviors, while FA attenuated the effects of Nic withdrawal on anxiety and depression as well as Bup. In support, the biochemical results demonstrated a balance between oxidant and antioxidant mediators in addition to the increase and decrease of serotonin and monoamine oxidase (MAO) activity in cortical tissue. TNF-α as an inflammatory agent was decreased, whereas IL-10 as an anti-inflammatory parameter was increased. Conclusions The present findings suggest anxiety and depression caused by Nic withdrawal were attenuated by FA more likely through the reduction activity of MAO, the important enzyme responsible for serotonin metabolism along with balance between oxidant/antioxidant and pro-inflammatory/anti-inflammatory mediators. However, various mechanisms might be involved, which requires further investigation. Implications Nic withdrawal-induced depression and anxiety like behavior in rats followed by neuro-oxidative damage and neuro-inflammation. FA supplementation as well as Bup improved cognitive disorders induced by Nic withdrawal by increasing neuro-inflammation and neuro-oxidative damage. [ABSTRACT FROM AUTHOR]

Kidney diseases are one of the common diseases, which are one of the main causes of death in society and impose costs on the health system of the society. A growing body of evidence has well documented that inflammatory responses and oxidative damage play a significant role in the progress of various kidney diseases. This study examined whether selenium (Sel) could prevent the detrimental influences of lipopolysaccharide (LPS) in rats. Four groups of Wistar rats were considered: control, LPS (1 mg/kg, i.p., for 14 days), LPS–Sel 1 (0.1 mg/kg, i.p., for 14 days), and LPS–Sel 2 (0.2 mg/kg, i.p., for 14 days). Sel treatment markedly attenuated oxidative stress damage in the kidney tissue in LPS-induced renal toxicity. Generally, the administration of Sel resulted in improved antioxidant indicators such as catalase (CAT) and superoxide dismutase (SOD) activities, or total thiol content, and decreased malondialdehyde (MDA) in the kidney tissue. It also decreased interleukin-6 in kidney homogenates. Furthermore, Se treatment significantly inhibited the elevation of serum biochemical markers of kidney function including serum, BUN, and creatinine. Based on the findings of the current study, it seems that the administration of Sel to LPS-treated rats improves renal function by reducing oxidative damage and inflammation in kidney tissue. However, more research is needed to reveal the accurate mechanisms for the effect of Sel on renal outcomes of LPS in human subjects. [ABSTRACT FROM AUTHOR]

Carvacrol is a phenolic monoterpenoid compound that has antibacterial, antifungal, anti-cancer, and anti-inflammatory effects. Lipopolysaccharide (LPS) is derived from the outer cell wall of gram-negative bacteria and is responsible for acute kidney injury. In this research, the protective effect of carvacrol on lipopolysaccharide-induced acute kidney injury was studied. For this purpose, 40 male Wistar rats (200-250 g) were used. Animals were randomly divided into 5 equal groups: 1) control, 2) LPS group, 3) LPS+carvacrol (25 mg kg-1), 4) LPS+carvacrol (50 mg kg-1) and 5) LPS+carvacrol (100 mg kg-1). To induce acute renal injury, daily 1 mg kg-1 LPS for 2 weeks was injected intraperitoneally. Carvacrol was administered intraperitoneally daily for 30 minutes before LPS injection. LPS-induced kidney injury was evaluated by blood urea nitrogen (BUN), serum creatinine, and nitric oxide levels in kidney tissue by spectrophotometry methods. The level of the interleukin 1 beta was detected by ELISA in the kidney. Our results showed that LPS injection increased BUN, creatinine, nitric oxide, and IL-1β levels (P <0.001). Pretreatment with carvacrol reduced BUN at 25 mg kg-1 (P <0.001), 50 mg kg-1 (P <0.01), and 100 mg kg-1 (P <0.001) doses, nitric oxide at 25 mg kg-1 (P <0.05), 50 mg kg-1(P <0.01) and 100 mg kg-1(P <0.001) doses, and IL-1β levels (P <0.001) at all doses significantly but did not affect serum creatinine. These results indicate that carvacrol has an antiinflammatory effect and protects kidneys against LPS by reducing pro-inflammatory mediators such as IL-1β and nitric oxide. [ABSTRACT FROM AUTHOR]

Objective(s): The present study aimed to assess the efficacy of some known extracts on learning and memory impairment induced by streptozocin (STZ) in male rats. Materials and Methods: Eighty male rats were randomly divided: 1) control, 2) STZ (50 mg/kg), 3) STZ+Trigonella foenum-graecum (200 mg/kg), 4) STZ+Ribes rubrum (500 mg/kg), 5) STZ+Lavandula angustifolia (400 mg/kg), 6) STZ+Arctium Lappa (200 mg/kg), 7) STZ+mix of extracts (quarter dose of each extract), and 8) STZ+metformin (100 mg/kg). Treatment was continued for 8 weeks and the after that, the behavioral tests related to learning and memory including Morris water maze (MWM) and passive avoidance (PA) were performed along with biochemical analysis associated with oxidative stress pathway and other related indicators. Results: According to the results, all extracts demonstrated potential effect to ameliorate cognitive impairment caused by STZ in both MWM and PA tests along with attenuating oxidative stress indicators like malondialdehyde (MDA), while total thiol content and anti-oxidant enzyme activity like superoxide dismutase (SOD) and Catalase (CAT) remarkably increased in biochemical test results. Interestingly, the mixture of extracts illustrated much better results in ameliorating the brain-derived neurotrophic factor (BDNF), while attenuating the amyloid-B and glial fibrillary acidic protein (GFAP). Conclusion: The present study demonstrated these extracts alone or in combination with a minimum dose have a strong potential to ameliorate learning and memory impairment induced by STZ along with lowering glucose levels by which they prevent or manage diabetes. It is noteworthy that the results matched those of metformin a well-known anti-diabetic drug. [ABSTRACT FROM AUTHOR]

The present study focused on examining the impact of vitamin C (Vit C) administration on the function of memory and the status of oxidative stress (OS) in the hippocampal area of the brain using an unpredictable chronic mild stress (UCMS) model in rats. To this end, 50 male Wistar rats (11-12 weeks of age at the start of the study) were assigned to five groups of six animals, including control, UCMS, UCMS + Vit C 50 mg/Kg, UCMS + Vit C 100 mg/Kg, and UCMS + Vit C 400 mg/Kg. The animals received daily intraperitoneal injections of Vit C at a certain time (9 am) before the initiation of a stressor. UCMS, including a progression of typical stressors, was applied for four weeks. Subsequently, using the passive avoidance (PA) and Morris water maze (MWM) tests were performed to investigate learning and memory. Eventually, hippocampal tissues were evaluated in terms of OS criteria. The results revealed that the latency to enter the dark chamber (P < 0. 01 and P < 0.05, PA test) and the time spent in the target quadrant (P < 0.0001, MWM test) were shorter in the UCMS group, while latency to discover the platform was longer (P < 0.05 and P < 0.001, MWM test) compared to the control group. However, UCMS decreased the content of thiol (P < 0.0001), as well as the activities of catalase (P < 0.0001) and superoxide dismutase (P < 0.0001), whereas the concentration of malondialdehyde (P < 0.01) increased in the hippocampal region of the brain in comparison to the control group. Interestingly, Vit C treatment reversed the mentioned effects of UCMS. Therefore, the latency to enter the dark chamber (P < 0. 05 and P < 0.01,1 and 24 h after the shock, PA test, UCMS + Vit C 400) and the time spent in the target quadrant (P < 0. 01 and P < 0.05, MWM test, UCMS + Vit C 400 and UCMS + Vit C 100, respectively) were longer in the UCMS + Vit C groups. Moreover, Vit C increased the content of thiol (P < 0.05, UCMS + Vit C 400), as well as the activity of catalase (P < 0.001, UCMS + Vit C 400) and superoxide dismutase (P < 0.0001, UCMS + Vit C 400, UCMS + Vit C 100), whereas the concentration of malondialdehyde (P < 0. 05 and P < 0.01, UCMS + Vit C 100, UCMS + Vit C 400) decreased in the hippocampal region of the brain in comparison to the UCMS group. Overall, these results suggest that Vit C could reverse UCMS-induced learning and memory impairment possibly through the modulation of brain OS. Key points Memory and learning impairments were induced by unpredictable chronic mild stress (UCMS) Vitamin C could prevent cognitive impairments caused by UCMS in rats by attenuation of oxidative stress in the brain. [ABSTRACT FROM AUTHOR]

Objective. We investigated the effects of hydroalcoholic extract of Nigella sativa (NS) on renal tissue oxidative damage associated with propylthiouracil (PTU)-induced hypothyroidism during neonatal and juvenile growth in rats.