Effect of Qingfei Huatan Huoxue Decoction combined with azithromycin on pulmonary function and inflammatory factors in children with Mycoplasma pneumonia.

To investigate the effect of Qingfei Huatan Huoxue Decoction combined with azithromycin on pulmonary function and inflammatory factors in children with Mycoplasma pneumonia. A total of 155 children with Mycoplasma pneumonia of toxic heat blocking lung syndrome were randomly divided into the control group (n=77) and the observation group (n=78) from March 2020 to March 2021. Both groups of children were given conventional treatment and azithromycin intravenous drip and the observation group was additionally given oral administration of Qingfei Huatan Huoxue Decoction, with 7 days as a course of treatment totaling 2 courses. The lung function, inflammatory factor level, immune function and coagulation function were compared between the two groups before and after treatment. After treatment, the symptom integral of fever, cough and pulmonary wet rales in the two groups were reduced, while FEV1, PEF and FEV1/ FVC were significantly increased, serum TNF-α, IFN- γ and IL-6 were significantly reduced, the levels of Immunoglobulin M (IgM), IgG and IgA were significantly reduced and plasma PT and APTT were significantly reduced, with more significant changes observed in the observation group (all P<0.05). The disappearance time of fever, cough and pulmonary moist rales in the observation group was significantly shorter than that in the control group (P<0.05). The recovery rate of the observation group was significantly higher than that of the control group (P<0.05). Qingfei Huatan Huoxue Decoction combined.

The inhibition of Platycodin D on Mycoplasma pneumoniae proliferation and its effect on promoting cell growth after anti-Mycoplasma pneumoniae treatment.

Platycodin D, extract from the root of Platycodon grandiflorum, is one of the most important monomers of the Qinbaiqingfei pellets (Qinbai) that has already been approved as the first Traditional Chinese Medicine for clinic use as an anti-M. pneumoniae agent. Qinbai constituents Scutellaria baicalensis and Platycodon grandiflorum were used to treat thousands of patients clinically in China each year. In this study, a M. pneumoniae-infected mouse strain, BALB/c, and a human-derived epithelial cell line, A549 type II pneumocytes, were used as experimental model. Anti-M. pneumoniae effect of Platycodin D was measured by the Real-time quantitative PCR, while the cell pathological change with hematoxylin and eosin and the growth recovery effects were determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Trypan Blue dye in the experimental model after M. pneumoniae infection. Our research results showed that Platycodin D could significantly inhibit M. pneumoniae and promote cell growth after anti- M. pneumoniae treatment in the infected cells or mice.

Treatment of experimental chronic pulmonary mycoplasmosis.

Mycoplasma pneumoniae infection has been associated with chronic lung disease. Treatment of chronic pulmonary mycoplasmosis has not been well investigated. BALB/c mice were intranasally inoculated once with M. pneumoniae or with sterile media (uninfected controls). Infected mice were treated with telithromycin or placebo daily for 10 days in the chronic phase of disease (18 months after inoculation). Mice (n=43) were evaluated before therapy and 1 day after completion of telithromycin. Treatment of infected mice with telithromycin at 18 months after infection significantly reduced chronic pulmonary histological inflammation compared with infected mice given placebo; however, this treatment did not improve airway obstruction or airway hyperresponsiveness. Therapy longer than 10 days may be necessary to improve pulmonary function.

Protective effects of the glutathione redox cycle and vitamin E on cultured fibroblasts infected by Mycoplasma pneumoniae.

The role of the glutathione (GSH) redox cycle and vitamin E as antioxidant defense systems was studied in normal human cultured skin fibroblasts infected by virulent Mycoplasma pneumoniae. In cells infected for 20 h, catalase activity was inhibited by 75% and the intracellular GSH decreased to 32% of its normal values. GSH peroxidase and oxidized glutathione (reductase activities in the infected cells were unaffected.) GSSG glutathione in the medium of the infected cells rose in accordance with the intracellular GSH decrease. The observed elevation in GSSG/GSH ratio was attributed to the increase in intracellular H2O2 content in M. pneumoniae-infected cells due to the marked inhibition in their catalase activity. The protective effect of the GSH redox cycle in infected cells was studied by depletion of cellular GSH, prior to their infection with M. pneumoniae, using buthionine sulfoximine (BSO), a selective inhibitor of gamma-glutamyl cysteine synthetase. After 16 h of incubation with BSO, the GSH levels were reduced to 38% of their normal value and recovered to 55% during 24 h after removal of the inhibitor. BSO had no effect on GSH peroxidase and catalase activities in either infected or noninfected cells. The level of malonyldialdehyde (an indicator of membrane lipid peroxidation) in BSO-treated cells infected by M. pneumoniae was 1.8 times higher than in infected controls. Cells enriched with 0.25 and 2.25 micrograms of vitamin E per mg of protein prior to their infection by M. pneumoniae revealed the following: a lesser degree of catalase inhibition, 46 and 30%, respectively, versus 64% in infected control cells that were not supplemented with vitamin E; lower levels of malonyldialdehyde, 55 and 20% increments, respectively, versus a 140% increment in infected controls; higher residual activity of lactate dehydrogenase, 76 and 96%, respectively, versus 58% in infected controls. Our data indicate that the oxidative damage induced in M. pneumoniae-infected cells due to the increase in intracellular levels of H2O2 and O2- is limited by the host cell GSH redox cycle and by supplementation with vitamin E.