Chronic Kombucha Beverage Consumption Attenuates Inflammatory Markers and Histopathology of Brain Tissue in Transnet Global Brain Ischemia in Rats.

There is evidence that kombucha beverage (KB), a traditional fermented beverage, has a preventive effect on experimental brain ischemia. According to our previous studies, pre-treatment of KB attenuates brain edema and improves motor skills and oxidative stress in a rat model of global brain ischemia. This study was designed to evaluate the effects of the pre-treatment of KB, as a novel agent, on pro-inflammatory parameters and brain histopathology changes following global brain ischemia. Adult male Wistar rats were randomly divided into the sham, the control, and the groups treated with kombucha (KB1 and KB2 groups). KB at doses 1 and 2 mL/kg was prescribed two-week consecutive days before induction of global brain ischemia. Global brain ischemia was induced by blocking common carotid arteries for 60 min and the following reperfusion by 24 h. The serum and brain levels of tumor necrosis factor-α(TNF-α), IL-1ß, histopathological change, and infarct volume are determined using the ELISA, hematoxylin and eosin (H&E), and 2,3,5-triphenyl tetrazolium chloride (TTC) staining, respectively. This study indicated that pre-treatment of KB significantly reduced infarct volume, the serum, and brain levels of TNF-α and IL-1ß. The histopathological finding of the brain tissue confirmed a protective role for pre-treatment KB in the ischemic rats. Thus, the present study showed that the beneficial effects of KB pre-treatment on brain ischemic may be mediated by decreasing pro-inflammatory parameters.

Effect of aminoguanidine on post-ischemic brain edema in transient model of focal cerebral ischemia.

Previous experimental studies have shown that aminoguanidine (AG) is beneficial in the late phase of cerebral ischemia. Recently, it has been reported that AG reduces cerebral edema in traumatic brain injury. However, the effects of AG on post-ischemic cerebral edema and blood-brain barrier (BBB) permeability are not clear. Under chloral hydrate anesthesia, transient focal cerebral ischemia was induced in rats by 60 min of middle cerebral artery occlusion (MCAO), followed by 23 h of reperfusion. Saline as vehicle or AG at the doses of 75, 150 and 300 mg/kg, i.p., was administered at the beginning or at 1 or 3 h after induction of ischemia. Subsequently, 24 h after MCAO brain edema, BBB permeability and infarct volume were evaluated. Administration of AG (150 mg/kg) at the beginning or at 1 or 3 h after MCAO, significantly reduced cerebral edema (P<0.001), while AG at the doses of 75 and 300 mg/kg had no effect. Moreover, treatment with AG (150 mg/kg) significantly reduces Evans Blue extravasation by 48% into ischemic brain compared to the saline group (P<0.001). Additionally, AG at the doses of 75 and 150 mg/kg significantly reduces cortical and striatal infarct volumes (P<0.001), while AG at the dose of 300 mg/kg did not change striatal infarct volumes (P>0.05). Our findings show that AG significantly reduced post-ischemic increase of brain edema with a 3-h therapeutic window in the transient model of focal cerebral ischemia. Moreover, it seems that at least part of the anti-edematous effects of AG is due to decrease of BBB disruption.