Effects of central FGF21 infusion on the glucose homeostasis in rats (brain–pancreas axis)

© 2023 Informa UK Limited, trading as Taylor & Francis Group.Introduction: Glucose homeostasis is a physiological process mediated by a variety of hormones. Fibroblast growth factor (FGF) 21 is a protein expressed in the liver, adipose tissue, muscle and pancreas and exerts actions in multiple targets including adipose, liver, pancreas and hypothalamus. The aim of this study was to examine the possible involvement of FGF21 in pancreatic and central control of glucose by measuring reflective changes in the release of insulin and glucagon. Methods: Thirty adult male Wistar Albino rats were divided; Control, PD + aCSF, PD + FGF21 groups (n = 10). Effects of intracerebroventricular (icv) FGF21 administration to pancreatic denervated (PD) rats. Agouti-related protein (AgRP), Pro-opiomelanocortin (POMC) levels and blood glucose homeostasis were investigated. Results: Administration of FGF21 to 3rd ventricle increased food consumption but body weight didn’t change significantly. AgRP level increased, pancreatic insulin levels increased, and glucagon level decreased. Conclusion: Central FGF21 administration is effective in regulating blood glucose homeostasis by increasing the amount and efficiency of insulin and changing glucose use

Differential expression of miRNAs related to autophagy pathway in tissue and serum samples of colorectal cancer patients

© 2022. Bratislava Medical Journal. All Rights Reserved.BACKGROUND: This study was aimed to investigate the relationship of miR-17-5p, miR-30b, miR-30d, miR-216a and miR-216b associated with autophagy gene beclin 1, and beclin 1 gene with colorectal cancer (CRC). MATERIALS AND METHODS: Forty-seven patients with CRC and 50 healthy individuals with no cancer history were included in this study. In the serum, tumor and non-tumoral tissue samples of the CRC patients, and in the serum samples of the healthy subjects, expression levels of miRNAs were detected by qRT-PCR. The beclin 1 gene expression levels were determined by qRT-PCR, and protein levels were determined by Western blot method in tumor and non-tumor tissue samples of the patients. RESULTS: The miR-17-5p and miR-30d expressions were found to be higher in tumor tissue as compared to patient non-tumor tissues, while expressions of beclin-1, miR-30b and miR-216a were found to be lower. In addition, the beclin-1 protein levels were signifi cantly decreased in the tumor tissue as compared to those in the patient non-tumor tissues. The miR-30d expression was signifi cantly reduced in the serum of the patients when the serum samples of CRC patients and healthy controls were compared. CONCLUSION: The beclin 1 gene may play a role as a tumor suppressor in CRC. Moreover, these miRNAs cannot be used as highly reliable biomarkers in serum for CRC diagnosi

Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

As aim of this study, the knowledge of whether vinpocetine (VINPO) is cardioprotective or not following isoprotenol (ISO) induced cardiac ischemia in rats. In myocard infarction, the one of the responsible mechanisms of injury is oxidative damage and inflammmation. The effect of Vinpo which is the potent antioxidant and anti inflammatory agent aimed to reveal as the biochemical, electrophysiological, and histopathologic parameters. In this study, thirty- two Wistar-Albino male rats (in the estimated weight of 250-400gm.) were divided into four groups, each consisting of eight rats. The group 1 named as sham, no any drug used in this group. Group 2 named as iso group, only isoprotenol was adminestered, the group 3 named as vinpo and iso group, here initially vinpocetine then isopretenol were used, and the group 4 named as iso and vinpo, here initially isoprotenol then vinpocetine were used. For the rats in group 2, in first and second day isoprotenol adminestered at a dose of 120mg/kg using an intraperitoneal injection. At third and fourth day no any drug used. And at fifth day the experiment terminated. For the rats in group 3, at the first and second day Vinponcetine adminestered at adose of 20 mg/kg using an intraperitoneal injection, after 30 minute isoprotenol administered at adose of 120mg/kg using an intraperitoneal injection. At third and fourth day no any drug was used. And at fifth day experiment was terminated. Lastly for the rats in group4, first and second day isoprotenol administered at adose of 120mg/kg using an intraperitoneal injection, at third and fourth day vinpocetine adminestered at adose of 20 mg/kg using an intraperitoneal injection, and at fifth day experiment terminated. Prior to termination of experiment the pulse rate and ECG changes were recorded. After completion of experiment protocols blood samples and cardiac tissue samples were recieved. For the knowledge of effects of vinpocetine experimental miyocardial ischemia induced in rats, and the serum myoglobulin, total creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanin aminotransferase (ALT), measured. In myocardial tissue as an antioxidative system and an oxidative stres markers; malonylaldehate (MDA), Superoxidedismutase (SOD), Catalase (CAT), Glutathionperoxidase (GPx), GSH, Total oxidant status (TOS),Total antioxidant status(TAS),Oxidative stres index (OSI) studied. As a result, Vinpocetin showed positive impact on cardiac functions. With all of these for the best clear results, advanced studies are needed. [Med-Science 2017; 6(4.000): 629-634

Protective effect of Nigella sativa oil against thioacetamide-induced liver injury in rats

antioxidant which is known to have liver protective effects, against thioacetamide (TAA)-induced liver injury. Accordingly, we aimed to investigate the toxicity of a hepatotoxic agent, thioacetamide, compared the NSO and NAC liver preventive effects in experimental animal model. Wistar-albino rats were randomly allocated to five groups, each consisting of eight rats, and were subjected to different treatment regimens for 6 days. Alanine aminotransferase (ALT), malondialdehyde (MDA), and protein carbonyl (PC) levels decreased significantly by NSO treatment (P [Med-Science 2017; 6(1.000): 96-103

Alpha lipoic acid decreases neuronal damage on brain tissue of STZ-induced diabetic rats

Neuropathy that develops due to diabetic complications causes cognitive impairment due to functional and structural damage. The aim of this study was to evaluate the biochemical, histological and physiological effects of Alpha Lipoic Acid (ALA) against brain tissue damage caused by diabetes. Fourty male Wistar albino rats were separated into four groups as control, diabetes mellitus (DM), ALA and DM+ALA. Single dose of 50 mg/kg intraperitonal streptozotocin (STZ) was used to induce DM. For six weeks, ALA (100 mg/kg/day) was administered to the ALA and DM+ALA groups. At the end of the six week rats were sacrificed by collecting blood samples and collected brain tissues (hippocampus, cortex, hippotalamus and striatum) were histologically evaluated in addition to the oxidant-antioxidant parameters. ALA administration showed significant improvement in cognitive functions evaluated by MWM in rats with diabetes mellitus (p < 0.05). SOD, CAT, GSH-Px activities, which were decreased in the DM group compared to the control group, increased statistically significantly in rats in DM+ALA group (p < 0.05). While MDA and PC levels increased in the DM group, they decreased statistically significantly in the DM+ALA group (p < 0.05). According to the histological examinations made by light and electron microscopies, it was determined that the ultrastructural damage and degeneration findings observed in the sections of the DM group were significantly ameliorated in the sections of rats in the DM+ALA group. ALA may be effective in restoring cell damage and cognitive functions in brain tissue with its antioxidant and neuroprotective effects without showing antidiabetic effects

Melatonin's protective effect on the salivary gland against ionized radiation damage in rats

Parlakpinar, Hakan/0000-0001-9497-3468; SIMSEK, GOKCE/0000-0001-5281-0986WOS: 000379928800009PubMed: 26757153ObjectivesThe aim of this study was to examine the effects of melatonin on ionized radiation-induced salivary gland damage using an experimental model. Materials and MethodsThirty-two rats were randomized into four groups: (i) the control group (C, n = 8) that received intraperitoneal (i.p.) 0.9% NaCl; (ii) the melatonin group (M, n = 8) that received i.p. 5 mg/kg melatonin; (iii) the radiotherapy group (RT, n = 8) that underwent irradiation; (iv) the melatonin plus radiotherapy group (M+RT, n = 8) that received i.p. 5 mg/kg of melatonin, followed by irradiation 30 min later; and (v) the radiotherapy plus melatonin group (RT+M, n = 8) that received irradiation followed by i.p. 5 mg/kg of melatonin 30 min later. The medications and irradiation were administered for 5 days and the salivary glands of the rats were excised 10 days later; the histopathological changes in the salivary glands were assessed and biochemical analyses were conducted (tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI)). ResultsRegardless of whether melatonin was administered before or after radiotherapy, melatonin decreased the radiation-induced parotid and submandibular histological damage. In addition, regardless of whether administration occurred before or after radiotherapy, melatonin decreased oxidative stress markers, such as MDA, TOS, and OSI. On the contrary, levels of antioxidative markers, such as CAT and GPx, were increased by melatonin. ConclusionsMelatonin may have a significant protective effect on salivary gland damage secondary to ionizing radiation

A comparative study on oxidative and antioxidative markers of serum and follicular fluid in GnRH agonist and antagonist cycles

To determine whether concentrations of oxidative stress markers of follicular fluid and serum are different in GnRH agonist protocol from GnRH antagonist protocol

Effects of molsidomine on retinopathy and oxidative stress induced by radiotheraphy in rat eyes

Parlakpinar, Hakan/0000-0001-9497-3468; OZER, MURAT ATABEY/0000-0003-1807-6911WOS: 000400977100023PubMed: 27897441Purpose: To determine the role of Molsidomine in preventing radiation-induced retinopathy after head and neck region irradiation of rats with a single radiation dose of 15 Gy. Materials and Methods: Male Wistar albino rats were randomly grouped into five as follows: (1) control group rats, which were applied through an intraperitoneal (i.p.) vehicle without radiotherapy (RT); (2) RT group rats received a single dose of 15 Gy irradiation and after daily 0.1 ml vehicle i.p. for 5 consecutive days; (3) molsidomine (MOL) group rats were treated for 5 consecutive days by i.p. with 4 mg/kg/day MOL; (4) irradiation plus MOL group (RT+MOL) rats received irradiation and after 10 days single daily i.p. dose of MOL for 5 consecutive days; and (5) MOL+RT group rats were treated for 5 consecutive days by i.p. with MOL before RT. At the end of the work the rats were sacrificed under high-dose anesthesia on the 16(th) day and then eye tissues were taken for histopathological, immunohistochemical (caspase-3), and biochemical analyses (superoxide dismutase [SOD], glutathione peroxidase [GSH], and malondialdehyde [MDA]). Results: RT significantly decreased both the content of GSH and the activity of SOD, and significantly increased the production of MDA level in the rat eyes. MOL treatment significantly increased the SOD and GSH levels and significantly decreased the MDA production (p < 0.0001). In addition, RT significantly increased the number of ganglion cells (GCs; p = 0.001), whereas especially pretreatment with MOL improved (p = 0.013). RT led to significant retinopathy formation, and MOL therapy protected the retina from radiation-induced retinopathy (p < 0.0001). Conclusions: We suggest that MOL is a powerful antioxidant and free radical scavenger that prevents the rat eyes from radiation-induced retinopathy and oxidative stress