Publications by authors named "Sinan Saral"

6 Publications

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Apelin-13 activates the hippocampal BDNF/TrkB signaling pathway and suppresses neuroinflammation in male rats with cisplatin-induced cognitive dysfunction.

Behav Brain Res 2021 Jun 15;408:113290. Epub 2021 Apr 15.

Recep Tayyip Erdogan University, Faculty of Medicine, Department of Biochemistry, Rize, Turkey. Electronic address:

It has been established that cisplatin causes neuronal damage and cognitive impairment. However, the mechanism is not sufficiently clear. Apelin-13 is an endogenous peptide with strong neuroprotective effects through the synthesis of neurotrophic factors and suppression of inflammation. The aim of this study was to investigate the role of brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) signaling pathway and the potential inhibitory effects of apelin-13 in the mechanism of cisplatin-induced hippocampal damage and cognitive impairment. Apelin-13 was administered to adult sprague dawley male rats at a dose of 20 nmol/kg every day for 4 weeks, cisplatin was administered at a dose of 5 mg/kg once a week for 4 weeks. The spatial and recognition memory tests of the rats were performed on the 5th week. BDNF and the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels were measured by ELISA in hippocampal homogenates. Pyramidal neuron and glial cell damage in the hippocampal CA1, CA3 and dentate gyrus (DG) were analyzed histologically. TrkB activity in the hippocampus was determined by immunohistochemical methods. Cisplatin impaired spatial and recognition memory in rats, while apelin-13 improved spatial memory but did not affect recognition memory. Cisplatin suppressed BDNF in the hippocampus while increased IL-1β and TNF-α. In contrast, apelin-13 administration increased BDNF but significantly suppressed TNF-α and IL-1B. Cisplatin caused pyramidal neuron and glial cell damage in CA1, CA3 and DG. In the cisplatin + apelin-13 group, however, pyramidal neuron and glial cell damage was less than those without apelin-13. Cisplatin increased TrkB activity in the hippocampus, which was counteracted by apelin-13. In conclusion, apelin-13 reduced the cisplatin-induced cognitive deficiency, by suppressing inflammation and stimulating the synthesis and activation of neurotrophic factors in hippocampal tissue.
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http://dx.doi.org/10.1016/j.bbr.2021.113290DOI Listing
June 2021

White Tea Reduced Bone Loss by Suppressing the TRAP/CTX Pathway in Ovariectomy-Induced Osteoporosis Model Rats.

Cells Tissues Organs 2020 19;209(1):64-74. Epub 2020 Jun 19.

Department of Radiology, Faculty of Medicine, Recep Tayyip Erdogan University, Rize, Turkey.

Osteoporosis is an important skeletal disease characterized by bone weakness and high risk of fracture in postmenopausal women. Tea consumption is known to play an important role in the prevention or alleviation of osteoporosis. However, the therapeutic effects of aqueous extracts of white tea (WT) have not been evaluated in osteoporosis rat models. The aim of this study was to investigate the potential anti-osteoporotic role of WT in ovariectomized (OVX) rats. WT was given orally at 0.5% w/v doses for 12 weeks in OVX rats. Biochemical parameters in blood samples, bone tartrate-resistant acid phosphatase (TRAP), C-terminal telopeptide of type 1 collagen (CTX) and estradiol levels were evaluated. Bone mineral density and bone mineral content values were measured in the left femur. In addition to histopathological examination, osteolcalcin, osteopontin and TUNEL levels were determined. OVX group data demonstrated that bone loss occurred by thinning of the metaphyseal growth plates of the femur. Similarly, the levels of TRAP and CTX, markers of osteoclastic activity, were found to be high concurrently with a decrease in femoral bone mineral density. In addition, increased osteolcalcin and osteopontin levels were present in the metaphyseal growth zones. On the other hand, while TRAP and CTX levels were suppressed in the OVX-WT group, bone mineral content increased. In ad-dition, TUNEL, osteocalcin and osteopontin positivity decreased in the right femoral metaphysis growth zones, proliferating zone and resting zone cells. These results showed that chronic WT consumption has a protective effect by reducing bone resorption in OVX-induced osteoporotic rats.
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http://dx.doi.org/10.1159/000507791DOI Listing
March 2021

The effect of white tea on serum TNF-α/NF-κB and immunohistochemical parameters in cisplatin-related renal dysfunction in female rats.

Biomed Pharmacother 2019 Apr 22;112:108604. Epub 2019 Feb 22.

Department of Histology and Embryology, Faculty of Medicine, Recep Tayyip Erdogan University, Rize, Turkey.

Objective: Nephrotoxicity is the most important side effect of the antineoplastic drug cisplatin, thereby restricting its use. The aim of this study was to investigate the protective effects of white tea infusions (WT) against renal damage induced by cisplatin (CP) in rats by biochemical and histopathological means.

Materials And Methods: This study used 24 female Sprague Dawley rats at 12-14 weeks of age and weighing 250-300 g. Rats were divided into three groups: Control, CP and CP + WT groups. CP was injected 7 mg/kg i.p as a single dose/rat in the CP group. White tea was given at a dose of 0.5% (w/v) for 4 weeks. At the end of the experiment, blood urea nitrogen (BUN), creatinine, uric acid, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nuclear factor kappa B (NF-κB) along with caspase-3 in the kidney were evaluated in study.

Results: BUN, creatinine, TNF-α, NF-κB and IL-6 levels of the CP group showed a statisically significant increase in comparison to the control group. TNF-α, NF-κB and IL-6 levels showed a statistically significant decrease in the CP + WT group with respect to the CP group. Caspase-3 levels in tubular epithelial cells decreased in CP + WT group compared with CP group (p = 0.02).

Conclusion: White tea infusions reduced significantly the nephrotoxicity of CP. The anti-nephrotoxic feature of the infusion may be attributed primarily to its anti-inflammatory and anti-apoptotic characteristics.
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http://dx.doi.org/10.1016/j.biopha.2019.108604DOI Listing
April 2019

The Effects of Hesperidin and Quercetin on Serum Tumor Necrosis Factor-Alpha and Interleukin-6 Levels in Streptozotocin-induced Diabetes Model.

Pharmacogn Mag 2018 Apr-Jun;14(54):167-173. Epub 2018 Apr 10.

Department of Physiology, Faculty of Medical School, Recep Tayyip Erdogan University, Rize 53000, Turkey.

Background: Diabetes mellitus (DM) is a metabolic disorder that occurs as a result of absolute or relative insufficiency of insulin release and/or insulin effect due to impairment of carbohydrate, fat and protein metabolism, and it is characterized by hyperglycemia and leads to various complications.

Objective: In this study, it was aimed to investigate the effects of (HP) and , which are natural flavonoids, on serum malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels in rats with streptozotocin (STZ)-induced diabetes.

Materials And Methods: The experimental animals were divided into four groups, each group comprising ten rats designated as follows: Group 1 served as control rats (C); Group 2 served as diabetic rats (DM); Group 3 served as diabetic rats administered HP (DM + HP) (100 mg/kg b. w.); and Group 4 served as diabetic rats administered (DM + Q) (100 mg/kg b. w.).

Results: Serum MDA and GSH levels were significantly higher in STZ-induced DM group than control group ( < 0.05). In DM + HP and DM + Q groups, MDA levels were significantly decreased compared to DM groups ( < 0.05), but there was no significant difference GSH levels between DM, DM + HP, and DM + Q groups ( > 0.05). TNF-α levels in STZ-induced DM group were significantly decreased compared to control group ( < 0.05), and groups of DM + HP and DM + Q had higher serum TNF-α levels than STZ-induced DM group ( < 0.05). In STZ-induced DM group, serum IL-6 levels were decreased compared to control group ( < 0.05).

Conclusion: As a result, in this study, we determined that HP and may play an effective role in regulating insulin metabolism metabolism in diabetes. However, considering the incompatibility of various results in the literature as well as our own results, we think that the actual role of cytokines in the pathogenesis of diabetes is one of the issues that need to be clarified in further studies.

Summary: (HP) and reduced the insulin, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and malondialdehyde (MDA) serum levels and raised the glutathione (GSH) levels compared to diabetes mellitus (DM) groupSZT-induced increased the MDA serum levels and decreased the GSH levels compared to control groupHP and -treated rats showed higher interleukin-6 and tumor necrosis factor alpha cytokine levels than DM groupHP and may play an effective role in regulating insulin metabolism in diabetes. DM: Diabetes mellitus, MDA: Malondialdehyde, GSH: Glutathione; IL-6: Interleukin-6, TNF-α: Tumor necrosis factor alpha, HP: Hesperidin, Q; Quercetin, STZ: Streptozotocin, TC: Total cholesterol, TG: Triglyceride, HDL-C: High density lipoprotein cholesterol, LDL-C: Low density lipoprotein cholesterol, VLDL-C: Very-low-density lipoprotein cholesterol.
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http://dx.doi.org/10.4103/pm.pm_41_17DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5909310PMC
April 2018

The effect of hesperidin and quercetin on oxidative stress, NF-κB and SIRT1 levels in a STZ-induced experimental diabetes model.

Biomed Pharmacother 2017 Jun 7;90:500-508. Epub 2017 Apr 7.

Guneysu Vocational School of Physical Therapy and Rehabilitation, Recep Tayyip Erdogan University, Rize 53000, Turkey. Electronic address:

Objective: The aim of this study is to investigate the roles of SIRT1 and NF-κB in the pathogenesis of diabetes mellitus in rats with STZ-induced diabetes and determine the effects of hesperidin and quercetin on oxidative stress and on the levels of SIRT1 and NF-κB.

Materials And Methods: The experimental animals were divided into four groups, each group comprising ten rats designated as follows: group 1 served as control rats (C); group 2 served as diabetic rats (DM); group 3 served as diabetic rats administered hesperidin (DM+HSP) (100mg/kg b.w.) in aqueous suspension orally for 15 days; and group 4 served as diabetic rats administered quercetin (DM+Q) (100mg/kg b.w.) in aqueous suspension orally for 15 days.

Results: In diabetic group, liver and kidney SIRT1, SOD and CAT activities were significantly lower than control group (p<0.05). Hesperidin and quercetin caused significant increase in the SIRT1, SOD and CAT activities of both DM+HP and DM+Q groups kidney tissues compared to DM group (p<0.05). Liver SOD activies were not found to differ significantly between DM, DM+Q and DM+HP groups (p>0.05). In DM+HP group, liver CAT activities were significantly higher than DM (p<0.05), but there was no significant difference in liver CAT activities between DM and DM+Q (p>0.05). In diabetic group, liver and kidney NF-κB and MDA levels were increased compared to control group (p<0.05), and groups of DM+HP and DM+Q had lower NF-κB and MDA levels than diabetic group (p<0.05).

Conclusion: As a conclusion, based on the results we obtained from this study and the literature data discussed above, we determined in STZ-induced diabetic rats that, increased glucose levels and liver and kidney damage markers decreased significantly after administration of hesperedin and quercetin, and that oxidative stress and NF-κB levels increased while SIRT1 levels decreased in the diabetic group.
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http://dx.doi.org/10.1016/j.biopha.2017.03.102DOI Listing
June 2017

Effects of apelin-13 in mice model of experimental pain and peripheral nociceptive signaling in rat sensory neurons.

J Recept Signal Transduct Res 2016 13;36(3):243-7. Epub 2015 Oct 13.

c Department of Physiology , Faculty of Medicine, Karadeniz Technical University , Trabzon , Turkey.

Objective: Apelin-13 is an endogenous peptide with potential analgesic action, although the sites of its analgesic effects remain uncertain and the results are even controversial with regard to its pain modulating action. This study evaluated the possible pain-modulating action of peripherally administered apelin-13 using heat-induced, withdrawal latency to the thermal stimuli, acute pain model in mice. Involvement of peripheral mechanisms was tested, by using the intracellular calcium concentrations as a key signal for nociceptive transmission, in cultured rat dorsal root ganglion (DRG) neurons.

Methods: DRG neurons were cultured on glass coverslips following enzymatic digestion and mechanical agitation, and loaded with the calcium-sensitive dye Fura-2 acetoxymethyl ester (1 µM). Intracellular calcium responses in individual DRG neurons were quantified by ratiometric calcium imaging technique.

Results: Peripheral injection of a single dose of apelin-13 (100 mg/kg and 300 mg/kg) significantly decreases the latency to painful stimuli in a dose and time-dependent manner (p < 0.01, p < 0.05, respectively, n = 8 each). Apelin-13 (0.1 µM and 1 µM) did not produce a significant effect on cytoplasmic Ca(2+) ([Ca(2+)](i)) responses, evoked by membrane depolarization, in cultured rat DRG neurons.

Conclusion: Together these results indicate that apelin-13 can cause increased pain sensitivity after peripheral administration, but this effect does not involve calcium mediated signaling in primary sensory neurons.
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http://dx.doi.org/10.3109/10799893.2015.1080274DOI Listing
October 2016