Context: Both copper and betanin have been implicated as having significant bioactivity against ischemic damage in a variety of experimental and clinical settings. The aim of this study is to investigate whether betanin and copper have any protective effect on spinal cord in an ischemia–reperfusion (I/R) model in rats. Design: Spraque-Dawley rats were used in four groups: Sham group (n = 7), control group (laparotomy and cross-clamping of aorta, n = 7), betanin treatment group (dosage of 100 mg/kg of betanin administered intraperitoneally (i.p.) 60 min before laparotomy, n = 7), copper sulfate treatment group (administered copper sulfate i.p. at a dose of 0.1 mg/kg/day for 7 days before laparotomy, n = 7). Malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) and superoxide dismutase (SOD) activity were measured. Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay was also performed to evaluate apoptosis. Setting: Kafkas University, Faculty of Medicine, Kars, Turkey. Results: I/R injury was successfully demonstrated with the surgical model. Betanin and copper treatment significantly decreased MDA levels, MPO activity and the number of apoptotic cells in the spinal cord. Betanin and copper treatment significantly increased GSH levels. Copper treatment significantly increased SOD activity, whereas betanin was not as effective. Apoptotic cells were significantly decreased in both treatment groups. Conclusion: I/R injury of the spinal cord can be successfully demonstrated by aortic clamping in this surgical model. Betanin/Copper sulphate has ameliorative effects against operative I/R injury. Low toxicity of those agents makes them ideal targets for clinical research for this purpose.

Rencuzogullari I, et al. Korean Circ J. 2016 Sep;48:e8. https://doi.org/10.4070/kcj.2017.0058

Objective: The aim of this study is to determine protective/modulatory effects of betanin in a femoral artery vasospasm model in rats. Materials and Methods: Sprague-Dawley rats were divided into three groups. Group 1: sham (n = 7), group 2: vasospasm model only (n = 7), group 3: postoperative betanin treatment in the vasospasm model (n = 7). 100 mg/kg betanin was administered orally to group 3 for 7 days, postoperatively. Peripheral blood malondialdehyde (MDA) and nitric oxide (NO) levels were measured for the quantification of oxidative stress, lumen diameter and wall thickness of femoral artery segments were determined to assess vasodilator effects of betanin. Results: Femoral artery vasospasm formation significantly increased both MDA (13.54 ± 3.09 mmol/mL) and NO levels (0.61 ± 0.06 µmol/mL) relative to the sham (9.07 ± 1.09 and 0.48 ± 0.1, respectively). Upon betanin administration, both MDA and NO approached baseline levels (9.95 ± 0.92 and 0.5 ± 0.06, respectively). Pathological examination of lumen diameter and wall thickness of the femoral arteries also revealed that betanin administration resulted in significant increase in lumen diameter when compared to vasospasm group (614.15 ± 245.77 versus 117.40 ± 46.19 µm) and decrease in wall thickness (64.68 ± 14.13 versus 96.73 ± 9.20 µm). Conclusion: Betanin was shown to have protective effect against oxidative stress in a peripheral artery vasospasm model in rats. It may also have a role in mitigating maladaptive changes in arterial structure, as shown in pathological examination.

The aim of this study was to evaluate complete blood cell count parameters including red blood cell indices, white blood cell subtypes, and platelet indices for predicting deep vein thrombosis (DVT). A total of 71 (44 male and 27 female)...

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