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    Protective Effects of Boron on Cyclophosphamide-Induced Bladder Damage and Oxidative Stress in Rats
    (HUMANA PRESS INC, 2020) Ayhancı, Adnan; Tanriverdi, Döndü Tuğçe; Şahintürk, Varol; Cengiz, Mustafa; Appak-Baskoy, Sıla; Şahin, İlknur Kulcanay
    This study aims to investigate protective effects of boron against cyclophosphamide-induced bladder toxicity that produces oxidative stress and leads to apoptosis of the cells. In total, 24 rats were divided into 4 equal groups. The control group received saline. The 2nd experimental group received 200 mg kg of cyclophosphamide i.p. on the 4th day while the 3rd group was given only boron (200 mg kg, i.p.) for 6 days. In the 4th group, boron was given for 6 days and cyclophosphamide (200 mg kg, i.p.) was administrated on the 4th day. Twenty-four hours after the last boron or cyclophosphamide administration, rats were sacrificed under anesthesia. Bladder tissues of rats were taken for histological and immunohistochemical (apoptotic markers such as caspase-3, bcl-2, and bax) and blood was taken for the biochemical (serum total thiol, serum natural thiol, serum thiol-disulfide) analysis. Transient epithelial thinning, edema, marked inflammatory reaction, and bleeding were observed in bladders of the group that received cyclophosphamide. Also, the activity of bax and caspase-3-positive cells increased while the number of bcl-2-positive cells decreased. In the same group, serum natural thiol and total thiol levels decreased while serum disulfide levels increased, which indicates oxidative stress. On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity. In parallel with the findings of this group, native thiol and total thiol levels increased and serum disulfide levels decreased pointing out to a decreased oxidative stress. Our results indicate that boron pretreatment significantly protects rat bladder against cyclophosphamide-induced bladder damage due to its antiapoptotic and antioxidant properties.
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    The role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats
    (Pergamon-Elsevier Science Ltd, 2022) Cengiz, Mustafa; Ayhancı, Adnan; Akkemik, Ebru; Şahin, İlknur Kulcanay; Gür, Fatma; Bayrakdar, Alpaslan; Cengiz, Betül Peker
    Introduction: This study aims to investigate whether boric acid (BA) can protect rats from acrylamide (AA)induced acute liver injury. Materials and methods: AA was used to induce acute liver injury. Thirty rats were divided into five group including Group 1 (saline), Group 2 (AA), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+AA) and Group 5 (20 mg/kg BA+AA). Their blood and liver were harvested to be kept for analysis. Liver function enzyme activities were performed by spectrophotometric method. Catalase (CAT), superoxide dismutase (SOD) activity, and malondialdehyde levels were determined by colorimetric method. The in-silico studies were performed using the blind docking method. Results: Administration AA to rats, biochemical parameters, liver histology, and expression levels of apoptotic markers were negatively affected. However, after the administration of BA, the altered biochemical parameters, liver histology, and expression levels of apoptotic markers were reversed. Moreover, the mechanisms of AA-induced deterioration in the levels of SOD, CAT, and Nrf2-Keap-1 and the mechanisms of the protective effect of BA against these deteriorations were explained by in silico studies. Conclusion: Thus, the present study could explain the interactions between AA and thiol-containing amino acid residues of Keap-1, the effect of BA on these interactions, and the biochemical toxicity caused by the AA. In this sense, this work is the first of its kind in the literature. Based on the biochemical, histopathological, and in silico results, it can be suggested that BA has the potential to be used as a protective agent against AA-induced liver injury.