Publications by authors named "Feng-ying Fu"

Unlabelled: C1q/tumor necrosis factor-related protein-3 (CTRP3) is a novel adipokine with modulation effects on metabolism, inflammation, and cardiovascular system. This study aimed to investigate the effect of CTRP3 on cardiac fibrosis and its underlying mechanism. The myocardial expression of CTRP3 was significantly decreased after myocardial infarction (MI).

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C1q/tumor necrosis factor-related protein-6 (CTRP6) is a newly identified adiponectin paralog with modulation effects on metabolism and inflammation. However, the cardiovascular function of CTRP6 remains unknown. This study aimed to determine its role in cardiac fibrosis and explore the possible mechanism.

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Adiponectin, an abundant adipose tissue-derived protein, exerts protective effect against cardiovascular disease. Adiponectin receptors (AdipoR1 and AdipoR2) mediate the beneficial effects of adiponectin on the cardiovascular system. However, the alteration of AdipoRs in cardiac remodeling is not fully elucidated.

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Background: Ischemic preconditioning (IPC) can reduce ischemia/reperfusion (I/R) injury in multiple organs and species. However, the effect of IPC on transplanted submandibular glands remains unknown. We explored the protection of IPC in transplanted submandibular glands in the rabbit and the underlying mechanism.

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Objective: To investigate the effect of parasympathectomy on secretion of submandibular glands and the feasibility of treatment for xerostomia in rats.

Methods: Twenty Sprague-Dawley male rats weighing 200 - 300 g were randomly divided into the experimental group (n = 12), in which the right chorda-lingual nerve was cut, and the control group (n = 8). The secretion of submandibular gland was measured for 5 min by Schirmer test for both groups.

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Aims: Adiponectin is considered an important adipokine protecting against diabetes, atherosclerosis, and cardiovascular disease. Because adiponectin receptors (AdipoRs) are critical components in the adiponectin signalling cascade, we investigated the effect of insulin on the expression of myocardial AdipoRs and explored the possible molecular mechanism.

Methods And Results: The hyperinsulinaemia rat model was induced by infusion of insulin (1 U/day) for 28 days: serum and myocardial adiponectin levels were increased, and skeletal muscle and myocardial AdipoR1 expression and AMP-activated protein kinase (AMPK) phosphorylation were decreased.

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Objective: To investigate the effect of baicalin on pulmonary functions and its mechanism during the development of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) in rats.

Methods: Rats were randomized into 5 groups: control, ARDS (OA induction, 0.12 mg/kg), baicalin-treated group (150 mg/kg), baicalin-treated group (300 mg/kg) and baicalin-treated group (450 mg/kg).

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Objective: To further test the protective effect of low-G pre-conditioning on +Gz stress induced cardiac damage.

Method: Forty-two male Wistar rats were randomly divided into 3 groups (n=14 for each group): group A (+1 Gz group), group B (+10 Gz group) and group C (low-G pre-conditioning group). The rats in group B were exposed to five +10 Gz plateaus of 30 s with 1 min intervals at +1 Gz, 3 times a week, for 3 weeks; while group A were only submitted to +1 Gz for 5 min.

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