Publications by authors named "He-quan Li"
Mannose has been reported to prevent acute lung injury (ALI), and mannose receptor (MR) has been demonstrated to have a role. The rationale for this study is to characterize the mechanism by which mannose and MR prevent lipopolysaccharide (LPS)-induced ALI. Male ICR mice were pretreated mannose by intravenous injection 5 min before and 3 h after intratracheal instillation of LPS.
View Article and Find Full Text PDF[Preventive effect of IL-18 gene modified mature dendritic cells vaccine on airway inflammation in mouse asthma model].
Zhejiang Da Xue Xue Bao Yi Xue Ban
March 2011
Objective: To investigate the preventive effect of interleukin-18 (IL-18) gene modified mature dendritic cells (mDC) vaccine on airway inflammation in mouse asthma model.
Methods: The asthma model was induced by injection of ovalbumin (OVA) in BALB/c mice. IL-18 gene modified mouse mature dendritic cells (mDC) were detected by flow cytometry and its capacity of inducing allogeneic T cell responses was examined by mixed lymphocyte reaction (MLR).
Article Synopsis
- The study investigates the impact of hemorrhagic shock and subsequent reperfusion on gastric mucosal injury in rats, comparing treatments with Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) against a saline control group.
- Results show that both SEF and CI significantly reduce the severity of gastric lesions compared to the saline group, evidenced by lower indexes of gastric mucosal lesions (IGML) and fewer severe lesions (grade 3).
- Additionally, treatments with SEF and CI were associated with decreased intracellular calcium levels and increased levels of certain prostaglandins, indicating a potentially protective effect on gastric mucosa following injury.
[The effect of a mouse IL-12 plasmid on airway inflammation and cytokine production in a mouse asthmatic model].
Zhonghua Jie He He Hu Xi Za Zhi
June 2003
Objective: To investigate the effect of a mouse IL-12 gene expressive plasmid (mIL-12 plasmid) on the airway inflammation and the cytokine production in asthmatic mice and to study the possible mechanisms.
Methods: A mouse model of asthma was established by sensitization with ovalbumin (OVA). Forty-one BALB/c mice were divided into six groups including an asthmatic model group (group A, eight mice, sensitized with OVA plus challenging with OVA by aerosol), a model control group (group B, six mice, sensitized with OVA plus aerosolizing with normal saline), a mIL-12 plasmid prevention group (group C, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 1, day 3, and day 5), a mIL-12 plasmid treatment group (group D, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 14, day 16, and day 18), an empty plasmid prevention group (group E, five mice, receiving intramuscularly empty plasmid 100 micro g on day 1, day 3, and day 5), and an empty plasmid treatment group (group F, six mice, receiving intramuscularly empty plasmid 100 micro g on day 14, day 16 and day 18).