The effect of Hippophae rhamnoides L. extract on acrylamideinduced brain injury in rats.

PURPOSE: Reactive oxygen species (ROS), interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1ß and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. METHODS: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. RESULTS: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1ß and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. CONCLUSIONS: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.

The effect of Hippophae rhamnoides L. extract on acrylamideinduced brain injury in rats

ABSTRACT Purpose: Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. Methods: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. Results: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. Conclusions: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.

Damage induced by paracetamol compared with N-acetylcysteine.

BACKGROUND: This study investigated the effect of thiamine pyrophosphate (TPP) on oxidative liver damage induced in rats with high-dose paracetamol. METHODS: Rats for this experiment were divided into the following groups: healthy control, paracetamol control, thiamine + paracetamol, TPP + paracetamol, and N-acetylcysteine + paracetamol. Oxidant and antioxidant parameters and liver function test levels were compared between the groups. RESULTS: The results show that TPP and N-acetylcysteine with paracetamol equally prevented a rise in oxidants such as malondialdehyde and nitric oxide. They also prevented a decrease in enzymatic and nonenzymatic antioxidants such as glutathione, glutathione peroxidase, glutaredoxin, glutathione S-transferase, superoxide dismutase, and catalase in the rat liver. CONCLUSION: Thiamine pyrophosphate and N-acetylcysteine had a similar positive effect on oxidative damage caused by paracetamol hepatotoxicity. These findings show that TPP may be beneficial in paracetamol hepatotoxicity.

Benefits of the antioxidant and anti-inflammatory activity of etoricoxib in the prevention of ovarian ischemia/reperfusion injury induced experimentally in rats.

AIM: This study is a biochemical investigation of the effect of etoricoxib, a selective cyclooxygenase (COX)-2 inhibitor, on ischemia/reperfusion (I/R) injury experimentally induced in rat ovaries. METHODS: Experimental animals were divided into four groups: (i) ovarian ischemia/reperfusion (IRG); (ii) 30 mg/kg etoricoxib + ovarian ischemia/reperfusion (EIRG-30); (iii) 60 mg/kg etoricoxib + ovarian ischemia/reperfusion (EIRG-60); and (iv) a sham operation (SG) control group. RESULTS: The results showed levels of malondialdehyde in the IRG, EIRG-30, EIRG-60 and SG group ovarian tissue of 20.2 ± 3.4, 11.2 ± 3.2, 5.5 ± 1.9 and 3.8 ± 1.5 µmol/g protein, respectively. Myeloperoxidase activity for these groups was 24.2 ± 6.7, 13 ± 2.4, 4 ± 1.8 and 3.5 ± 1.9 U/g protein, and total glutathione levels were 1.6 ± 0.8, 4.5 ± 1.9, 6.5 ± 1.9 and 7.5 ± 2.4 nmol/g protein, respectively. COX-1 activity in IRG, EIRG-30, EIRG-60 and SG group rat ovarian tissue was 5.0 ± 2.8, 12.2 ± 2.4, 16.7 ± 2.8 and 17.5 ± 4.7 U/mg protein, and COX-2 activity was 18.3 ± 2.7, 3.5 ± 1, 1.8 ± 0.7 and 0.7 ± 0.3 U/mg protein, respectively. CONCLUSION: Etoricoxib prevented oxidative damage induced with I/R in rat ovarian tissue. This property of etoricoxib suggests that it can be clinically beneficial in the prevention of damage that may arise with reperfusion by detorsion for the protection of the ovaries against torsion.

Effects of thiamine and thiamine pyrophosphate on epileptic episode model established with caffeine in rats.

This study examines the effect of thiamine (TH) and thiamine pyrophosphate (TPP) on epileptic episode model induced in rats with caffeine. Animals were divided into groups and given TH or TPP at doses of 10, 30 or 50mg/kg intraperitoneally. Subsequently, all animal groups were injected intraperitoneally with caffeine at a dose of 300mg/kg. Time of onset of epileptic episode was recorded, and the latent period was calculated in seconds. At the end of the experiment, tGSH and MDA levels and SOD and MPO enzyme activities in extracted brain tissues were measured. Latent period duration in rats in the control group was 134±3.2s, compared to 144±13.9, 147±14.5 and 169±15.1s, respectively, in the TH10, TH30 and TH50 groups and 184±8.54, 197±9.1, 225±8.37s, respectively, in the TPP10, TPP30 and TPP50 groups. Latent period duration was 236±6.7 in the diazepam group. Oxidant products were significantly lower in the TPP10, TPP30, TPP50 and diazepam groups compared to the control group (P<0.05), while SOD activity and tGSH levels were significantly higher (P<0.05). There was no significant difference between the TH10, TH30, TH50 groups and the control group in terms of oxidant and antioxidant levels (P>0.05). In conclusions, TPP, especially at a dose of 50mg/kg, significantly prolonged the latent period from administration of caffeine to time of episode and prevented oxidative damage.

Serum vitamin D levels in children with recurrent otitis media.

The aims of this study were to evaluate serum vitamin D levels in cases of recurrent otitis media and investigate the effect of vitamin D therapy on the risk of re-occurrence of the disease. This prospective study was performed by comparing serum vitamin D levels in children with recurrent otitis media and healthy children. Eighty-four children between 1 and 5 years of age and diagnosed with recurrent otitis media were enrolled as the study group. One hundred-and-eight healthy children with similar demographic characteristics were enrolled as the control group. Patients were divided into groups according to their serum 25(OH) vitamin D levels. In patients with low initial serum vitamin D levels, vitamin D therapy was administered in addition to conventional treatment for otitis media. Mean serum 25(OH) vitamin D level in the study group was 11.4 ± 9.8 ng/mL Serum 25(OH) vitamin D levels were below 20 ng/mL in 69 % (n = 58) of cases in this group. In the control group, mean serum 25(OH) vitamin D level was 29.2 ± 13.9 ng/mL and was below 20 ng/mL in 30 % (n = 32) of cases. Comparison of serum 25(OH) vitamin D levels and PTH in the study and control groups revealed a statistically significant difference (p < 0.05). Treatment was initiated in cases diagnosed with vitamin D deficiency, and patients were followed up in due course. The only episodes detected over the course of 1-year follow-up were one attack in five patients and two attacks in two. We believe that co-administration of supplementary vitamin D together with conventional treatments is appropriate in the management of upper respiratory infections such as otitis media.

The protective effect of thiamine pyrophosphate, but not thiamine, against cardiotoxicity induced with cisplatin in rats.

This study investigated the effect of thiamine pyrophosphate on oxidative damage associated with cardiotoxicity caused by cisplatin (CIS), an antineoplastic agent, in rats, and compared this with thiamine. Animals used in the study were divided into four groups of 6 rats each. These represented a control group receiving 5 mg/kg of CIS, study groups receiving 20 mg/kg of thiamine pyrophosphate plus 5 mg/kg of cisplatin (CTPG) or 20 mg/kg of thiamine plus 5 mg/kg of cisplatin and a healthy (H) group. All doses were administered intraperitoneally once a day for 14 days. Malondialdehyde, total glutathione and products of DNA injury results were similar in the CTPG and H groups (p > 0.05). Creatinine kinase, creatine kinase MB and troponin 1 levels were similar in the CTPG and H groups (p > 0.05). Thiamine pyrophosphate prevented CIS-associated oxidative stress and heart injury, whereas thiamine did not prevent these.

The effect of thiamine and thiamine pyrophosphate on oxidative liver damage induced in rats with cisplatin.

The aim of this study was to investigate the effect of thiamine and thiamine pyrophosphate (TPP) on oxidative stress induced with cisplatin in liver tissue. Rats were divided into four groups; thiamine group (TG), TPP + cisplatin group (TPG), healthy animal group (HG), and cisplatin only group (CG). Oxidant and antioxidant parameters in liver tissue and AST, ALT, and LDH levels in rat sera were measured in all groups. Malondialdehyde levels in the CG, TG, TPG, and HG groups were 11 ± 1.4, 9 ± 0.5, 3 ± 0.5, and 2.2 ± 0.48 µ mol/g protein, respectively. Total glutathione levels were 2 ± 0.7, 2.8 ± 0.4, 7 ± 0.8, and 9 ± 0.6 nmol/g protein, respectively. Levels of 8-OH/Gua, a product of DNA damage, were 2.7 ± 0.4 pmol/L, 2.5 ± 0.5, 1.1 ± 0.3, and 0.9 ± 0.3 pmol/L, respectively. A statistically significant difference was determined in oxidant/antioxidant parameters and AST, ALT, and LDH levels between the TPG and CG groups (P < 0.05). No significant difference was determined between the TG and CG groups (P > 0.05). In conclusion, cisplatin causes oxidative damage in liver tissue. TPP seems to have a preventive effect on oxidative stress in the liver caused by cisplatin.