Background Morbidity and mortality remain high for ischemic stroke victims, and at present these patients lack effective neuroprotective agents, which improve the cure rate. In recent years, studies have shown that pelargonidin has many biological actions. However, few studies are available regarding the pelargonidin treatment of cerebral ischemia. Methods The rat middle cerebral artery occlusion (MCAO) model was established to investigate the neuroprotective effect of pelargonidin on cerebral ischemia/reperfusion injury. Reperfusion was performed 2 h after ischemia; magnetic resonance imaging (MRI) and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining were used to measure the volume of cerebral ischemia. Both modified neurological severity scores (mNSSs) and Morris water maze test were used to assess the neurological functions. ELISA was applied to determine the levels of TNF-α, TGF-β, IL-6, IL-10, MDA, and SOD. The expression of Nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) protein in brain tissue was measured by immunofluorescence and Western blot assays. Results The results showed that pelargonidin could effectively reduce the volume of cerebral ischemia and improve the neurological function in MCAO rats, thereby improving memory and learning ability. With the corresponding decreases in the expression of TNF-α, TGF-β, IL-6, and MDA, the level of IL-10 and SOD increased and also promoted the nuclear metastasis of Nrf2 and the expression of HO-1 in ischemic brain tissues. Conclusions Our data demonstrated that pelargonidin ameliorated neurological function deficits in MCAO rats, and its potential mechanism of action was associated with overexpression of the Nrf2/HO-1-signaling pathway. This study will provide a new approach to treat cerebral ischemia/reperfusion injury.

ADC, f, and KDKI were identified as the most promising parameters for monitoring changes in rabbit liver VX2 carcinoma and f and ADC showed highest correlation with MVD. J. Magn. Reson. Imaging 2016;44:707-714.

Presence of intratumoral calcifications and vasculature can be potential prognostic features to screen patients for unfavorable prognosis.

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Background: Morbidity and mortality remain high for ischemic stroke victims and at present there are no effective neuroprotective agents to improve the cure rate for these patients. In recent years, studies have shown that pelargonidin has many biological actions including anti-oxidant, anti-inflammatory and anti-thrombogenic effects. However, there are few reports about the treatment of cerebral ischemia with this agent. Methods: The rat middle cerebral artery occlusion (MCAO) model was established to investigate the neuroprotective effect of pelargonidin on cerebral ischemia/reperfusion injury and to investigate its potential mechanism(s) of action. Magnetic resonance imaging and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining were used to measure the volume of cerebral ischemia and modified neurological severity score (mNSS), the Morris water maze test to assess neurological functions, and ELISA to determine the levels of inflammatory factors in serum including TNF-α, TGF-β, IL-6 and IL-10 and oxidative factors i.e. MDA and SOD. The expression of Nrf2 and HO-1 protein in brain tissue was measured by immunofluorescence and western blot assays. Results: The results showed that pelargonidin could effectively reduce the volume of cerebral ischemia and improve the neurological function in MCAO rats, thereby enhancing memory and learning ability. With corresponding decreases in the expression of TNF-α, TGF-β, IL-6 and MDA, pelargonidin increased the level of IL-10 and SOD and promoted the expression of Nrf2 and HO-1 proteins in ischemic brain tissues. Conclusions: Our datas demonstrated that pelargonidin ameliorated neurological function deficits in MCAO rats and its potential mechanism of action was associated with overexpression of the Nrf2/HO-1 signaling pathway, which may provide a new approach to the treatment of cerebral ischemia or cerebral ischemia/reperfusion injury.