Topiramate has protective effect on renal injury

Cüre, Medine Cumhur; Cüre, Erkan; Tümkaya, Levent; Kalkan, Yıldıray; Aydın, İbrahim; Kırbaş, Aynur; Efe, Hasan; Şehitoğlu, İbrahim; Yüce, Süleyman

doi:10.4149/bll_2015_050

Cited by 8 publications

(6 citation statements)

References 38 publications

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“…In humans, oral dose of TPM has been found to be effective within 2 hours in plasma and at target dose within 4 weeks (16). We chose 100 mg/kg/day of TPM and for 1 week since the previous animal studies used this dose and duration (17)(18)(19).…”

Section: Methodsmentioning

confidence: 99%

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

Kurt

Kalkan

Türüt

et al. 2018

Acta Med. (Hradec Kralove, Czech Repub.)

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A B ST R AC T Background: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. Materials and Methods: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. Results: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. Conclusions: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced. K E Y WO R D S Topiramate; ischemia-reperfusion; lung injury; tumor necrosis factor-alpha; endothelin-1

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Section: Methodsmentioning

confidence: 99%

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

Kurt

Kalkan

Türüt

et al. 2018

Acta Med. (Hradec Kralove, Czech Repub.)

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“…Reports regarding the effect of TOP on biosystem have been inconclusive. Some studies have documented the ameliorative effect of TOP on body organs (45)(46)(47). To the contrary, Khivsara et al (48) reported that TOP may induce toxicity in hepatic tissue.…”

Section: Discussionmentioning

confidence: 99%

The morphometrical and immunohistochemical investigation of the effect of topiramate on liver and the role of neuropeptide Y receptor in an obese female rat

Yahyazadeh¹,

Altunkaynak²,

Alkan³

2020

BLL

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OBJECTIVE: We aimed to investigate the possible effect of topiramate (TOP, 0.02 mg/kg/day) on the livers in a high-fat diet (HFD)-induced obesity rat model. The other objective was to evaluate the relationship between TOP administration and NPY level using anti-NPY1R antibody. METHODS: Twenty-four adult female Wistar albino rats were randomly assigned into four equal groups as follow: control (CONT), obese (OBS), TOP, and OBS+TOP. All liver samples were investigated using the stereological analysis, as well as immunohistochemical and histopathological examination. RESULTS: The total number of hepatocytes was signifi cantly decreased in the OBS+TOP group compared to the CONT group or the OBS group (p < 0.05). We found a signifi cant increase in the mean volume of liver in the OBS group compared to the CONT group (p < 0.05). Also, the mean volume of liver was signifi cantly decreased in the OBS+TOP group compared to the OBS group (p < 0.05). CONCLUSION: Taken together, our fi ndings suggest that decreased liver volume is possibly attributed to TOP administration via setting the NPY level in the obese rats. Further, the side effects of TOP in combination with health risk of obesity may have led to an increase in hepatotoxicity and the subsequent hepatocyte loss (Fig. 7, Ref. 56).

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“…Increased CA-II causes the conversion of surplus bicarbonate to carbonate radicals (29,30). Recent studies have suggested carbonate radicals to be the major mediator of various types of oxidative damage (31).…”

Section: Discussionmentioning

confidence: 99%