This study aims to prepare ultrasound-targeted glial cell-derived neurotrophic factor (GDNF) retrovirus-loaded microbubbles (M pLXSN-GDNF) to verify the properties of the microbubbles and to study the therapeutic effect of the GDNF retrovirus-loaded microbubbles combined with ultrasound (U) to open the blood–brain barrier (BBB) in a Parkinson’s disease (PD) model in rats, allowing the retrovirus to pass through the BBB and transfect neurons in the substantia nigra of the midbrain, thereby increasing the expression of GDNF. The results of western blot analysis revealed significant differences between U + MpLXSN-EGFP, U + M + pLXSN-GDNF, and M pLXSN-GDNF (P < 0.05) groups. After 8 weeks of treatment, the evaluation of the effect of increased GDNF expression on behavioral deficits in PD model rats was conducted. The rotation symptom was significantly improved in the U + MpLXSN-GDNF group, and the difference before and after treatment was significant (P < 0.05). Also, the content of dopamine and the number of tyrosine hydroxylase-positive (dopaminergic) neurons were found to be higher in the brain of PD rats in the U + M pLXSN-GDNF group than in the control groups. Ultrasound combined with GDNF retrovirus-loaded microbubbles can enhance the transfection efficiency of neurons in vivo and highly express the exogenous GDNF gene to play a therapeutic role in PD model rats.

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Background Floralozone (FL) is medicine with the refreshing aroma of rabbit's ear grass, which can be used to prevent the progression of atherosclerosis and reduces endothelial dysfunction. Vascular endothelial growth factor receptor 1 (VEGFR1) is one of the receptors of vascular endothelial factor (VEGF), which mainly plays a negative role in cardiovascular system regulation mainly by acting as a decoy receptor in endothelial cells. Therefore, the purpose of this study is to evaluate whether FL can down-regulate VEGFR1 expression in treating diabetes-induced heart failure (HF). Methods We used high-sugar and high-fat diet and tail vein injection of streptozotocin (STZ) to establish the rat model of HF. After intragastric administration of FL, the left ventricular function, pathological changes, oxidative stress condition in HF rats were assessed by echocardiography, oxidative stress monitoring, hematoxylin-eosin histological staining, argyrophilic staining, Masson staining, lichen red staining. The expression of VEGFR1 in the myocardial tissue of HF rats was detected by immunohistochemistry, immunofluorescence, western blot and RT-PCR analysis Results The HF model was established successfully. Through intragastric administration of FL, it was observed the cardiac function of HF rats was significantly improved, ventricular remodeling level was reversed, and the ability of antioxidant stress was enhanced. These therapeutic effects were closely connected with the down-regulation of VEGFR1 expression. ZM306416 is an antagonist of VEGFR1, which can up-regulate VEGFR1 expression and inhibit the protective effect of FL in rats with HF. Conclusions These results suggest that FL can play a salutary role in HF rats by down-regulating VEGFR1 expression, inhibiting ventricular remodeling and reducing oxidative stress.

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