History of epidemic control
China Journal of Chinese Materia Medica,2017,Vol 42,No. 08
Metabolomics on Pudilan Xiaoyan Oral Liquid in treatment of Influenza A/H1N1-induced pneumonia based on GC-MS
Chinese Traditional and Herbal Drugs,2018,Vol 49,No. 10
【Abstract】 Objective To screen the pneumonia-related abnormal metabolites in lung tissue of mice infected by Influenza A/H1N1, and to monitor the regulation effect of Pudilan Xiaoyan Oral Liquid (Pudilan) and to explore potential anti-pneumonia mechanism. Methods ICR mice were randomly divided into four groups with ten mice in each group: normal group, model group, Pudilan group, and Ribavirin group. The mice were infected with H1N1 virus intranasally and by gavage once every day for six consecutive days. 2 h after the last dose, the mice were sacrificed and lungs were collected. Metabolomics based on GC-MS was applied to analyze the changes of metabolites in the lung tissue of each group. The potential biomarkers of H1N1-induced pneumonia were screened out under three conditions of P < 0.05, VIP > 1.0, and Fold Change > 1.5. Metabolic pathways related to the treatment mechanism of Pudilan were analyzed. Results The infection of H1N1 virus led to infiltration of inflammatory cells in the lungs of mice and various degrees of pneumonitis and metabolic disorders. Pudilan and ribavirin both could ameliorate the symptoms of pneumonia and restore various metabolites back to the normal levels. Conclusion The treatment effect of Pudilan on H1N1-induced pneumonia is related to its regulatory effects on 14 potential biomarkers and 12 associated metabolic pathways.
Efficacy and mechanism of Lianhua Qingwen Capsules (LHQW) on chemotaxis of macrophages in acute lung injury (ALI) animal model
China Journal of Chinese Materia Medica,2019,Vol 44,No. 11
【Abstract】 This paper was mainly to discuss the potential role and mechanism of Lianhua Qingwen Capsules (LHQW) in inhibiting pathological inflammation in the model of acute lung injury caused by bacterial infection. For in vitro study, the mRNA expression of MCP-1 in RAW264.7 cells and THP-1 cells, the content of MCP-1 in cell supernatant, as well as the effect of LHQW on chemotaxis of macrophages was detected. For in vivo study, mice were randomly divided into seven groups, including normal group, model group (LPS 5 mg·kg −1), LHQW 300, 600, and 1 200 mg·kg −1 (low-, middle- and high-dose) groups, dexamethasone 5 mg·kg −1 group and penicillin-streptomycin group. Then, the anal temperature was detected two hours later. Dry weight and wet weight of lung tissues in mice were determined. TNF- α and MCP-1 levels in alveolar lavage fluid and MCP-1 in serum were detected. In addition, the infiltration of alveolar macrophages was also observed and the infiltration count of alveolar macrophages was measured with CCK-8 method. HE staining was also used to observe the inflammatory infiltration of lung tissues in mice. Both the in vitro and in vivo data consistently have confirmed that: by down-regulating the expression of MCP-1, LHWQ could efficiently decrease the chemotaxis of monocytes toward the pulmonary infection foci, thus blocking the disease development in ALI animal model.
Research Progress on Mechanism of Traditional Chinese Medicine in Treating Mycoplasma Pneumonia in Children
Chinese Archives of Traditional Chinese Medicine,2018,Vol 36,No. 06
【Abstract】 Mycoplasma pneumoniae pneumonia is a common respiratory disease in children, and macrolide drugs are the prior choice for clinical treatment. Macrolide drugs have been widely used for children’s respiratory diseases, leading to the increased resistance rate and gastrointestinal adverse reactions. Hence, more and more doctors begin to use traditional Chinese medicine (TCM) based on syndrome differentiation due to its obvious advantages. Studies have revealed that the efficacy of TCM in anti-MP is mainly related to the direct inhibition of MP, immune regulation, protection and repair of epithelial cells, microcirculation improvement, and reduction of adverse effects induced by western medicine.