Publications by authors named "Jiechen Zhu"

This study aimed to explore the profibrotic effects of chronic microaspiration of two major bile acids, including chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA), on lungs of rats at different stages, as well as the underlying mechanisms in vivo. A rat model was induced by weekly intratracheal instillation of DCA and CDCA. Our results showed that chronic microaspiration of bile acids resulted in alveolar structure disorder, and inflammatory cells infiltration in the pulmonary interstitium at the early stage.

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Background: Clinical studies have suggested nebulized budesonide (NB) as an alternative to systemic corticosteroids for patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). However, the optimal budesonide dose for AECOPD remains unclear.

Objectives: To compare the efficacy and safety of different doses of NB in the management of AECOPD.

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Background: Asthma is closely associated with tobacco smoking (TS) and is more difficult to effectively treat after exposure to TS.

Objective: To observe the effects of TS on the expression of endothelin-2 (ET-2) and airway inflammation in asthmatic rats and to explore the related mechanisms.

Methods: We established an animal model of asthma with ovalbumin (OVA)/Al(OH) and subjected different animal groups to TS and/or dexamethasone/bosentan.

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Background: Human BarH-like homeobox 2 (Barx2), a homeodomain factor of the Bar family, plays a critical role in cell adhesion and cytoskeleton remodeling, and has been reported in an increasing array of tumor types except non-small cell lung carcinoma (NSCLC). The purpose of the current study was to characterize the expression of Barx2 and assess the clinical significance of Barx2 in NSCLC.

Methods: Quantitative real-time polymerase chain reaction, immunohistochemistry and western blot analysis were used to examine mRNA and protein expression, respectively.

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Objective To investigate the effect of estrogen on the latent period of inducing asthma and airway inflammation in mice with asthma. Methods Forty male BALB/c mice were randomly divided into normal control group, OVA-induced asthma group, 400 μg/kg estradiol treatment group, 400 μg/kg estradiol combined with 7 mg/kg tamoxifen group, with 10 mice in each group. The OVA-induced asthma group, estradiol treatment group, and estradiol combined with tamoxifen group were sensitized and challenged by OVA; the normal control group was treated with normal saline instead.

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Objective: To investigate the expression of miR-199a-5p in airway smooth muscle cells (ASMCs) of rats in normoxia and hypoxia and its role in the regulation of proliferation and the expression of hypoxia inducible factor 1 alpha (HIF-1α) of ASMCs.

Methods: ASMCs were prepared by means of adherent culture in vitro. After ASMCs were cultured under normoxia and hypoxia conditions for 24 hours, the content of miR-199a-5p was detected by real-time quantitative PCR (qRT-PCR).

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Objective: To investigate the effect of leptin on the proliferation of airway smooth muscle cells (ASMCs) and the expressions of hypoxia-inducible factor-1α (HIF-1α) and nuclear factor-kappa B (NF-κB) of hypoxic rats.

Methods: The rat ASMCs were cultured under normoxic and hypoxic states. The hypoxic cells were divided into hypoxia group, leptin 50 μg/L hypoxia group (L50 group), leptin 100 μg/L hypoxia group (L100 group), leptin 200 μg/L hypoxia group (L200 group), leptin 200 μg/L and leptin receptor antibody hypoxia group (ob-R antibody group) by random number table.

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Objective: To evaluate the expression level of hypoxia-inducible factor-1α (HIF-1α) in the rat model of diet-induced obesity and asthma.

Methods: Forty male specific pathogen-free SD rats were randomly divided into four groups: normal body mass control group (group A), asthmatic rats with normal body mass (group B), obese control group (group C) and obese asthmatic rats (group D). The rats in both group A and B were fed basic diet, while those in group C and D were fed high-fat diet in order to establish diet-induced obese rat model.

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