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The gas temperature is a key parameter that affects the process of microwave plasma chemistry in industrial applications. Based on the molecular emission spectrometry of the A2Σ+→X2Πr electronic system of OH radicals, the gas temperature of the atmospheric air microwave plasma core at different absorbed microwave power levels, gas flow rates, gas humidities, and volume fractions of CO2 in air was analyzed. In the experiment, the absorbed microwave power, gas flow rate, gas humidity, and volume ratio of CO2 in air was varied from 560 to 1750 W, 10 to 24 l min−1, 30% to 95%, and 0% to 40%, respectively. Moreover, the axial gas temperature distribution of the plasma torch was measured. The experimental results showed that (i) the plasma gas temperature mainly ranged from 4000 to 7000 K, (ii) the plasma gas temperature rose with increasing absorbed microwave power but was hardly affected by the feeding gas flow rate, (iii) the plasma gas temperature decreased by ∼400 K for every 20% increase in the fraction of CO2 in air and decreased with increasing gas humidity, and (iv) the plasma torch gas temperature decreased along the axial direction. Due to the lack of a prevailing microwave discharge theory, an in-depth analysis of the mechanisms of gas temperature variation was performed based on the heat balance equation.

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Chronic obstructive pulmonary disease (COPD) is a serious chronic lung disease. Schisandrin A (SchA) is one of the most important active ingredients in Schisandra chinensis and has been used to treat various lung diseases in several countries. Here, we studied the pharmacological effect of SchA on airway inflammation induced by cigarette smoke (CS) and explored the therapeutic mechanism of SchA in COPD model mice. Our results showed that SchA treatment significantly improved the lung function of CS-induced COPD model mice and reduced the recruitment of leukocytes and hypersecretion of interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in bronchoalveolar lavage fluid (BALF). H&E staining showed that SchA treatment could effectively reduce emphysema, immune cell infiltration and airway wall destruction. In addition, we found that SchA treatment can stimulate the expression of heme oxygenase-1 (HO-1) through the nuclear factor-erythroid 2-related factor (Nrf2) pathway, significantly reduce oxidative stress, increase catalase (CAT) and superoxide dismutase (SOD) levels, and suppress the level of malondialdehyde (MDA) in COPD model mice. Moreover, SchA treatment suppressed the generation of the NLRP3/ASC/Caspase1 inflammasome complex to inhibit the inflammatory response caused by IL-1β and IL-18 and pyroptosis caused by GSDMD. In conclusion, our study shows that SchA treatment can inhibit the production of ROS and the activation of the NLRP3 inflammasome by upregulating Nrf-2, thereby producing anti-inflammatory effects and reducing lung injury in COPD model mice. More importantly, SchA exhibited similar anti-inflammatory effects to dexamethasone in COPD model mice, and we did not observe substantial side effects of SchA treatment. The high safety of SchA makes it a potential candidate drug for the treatment of COPD.

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