## 3 Results
### Lung Histopathological Inspections  
Significant sarcomomatous changes, including inflammatory cell infiltration-related thickening of the alveolar septum, thickening of secondary bronchus mucosa, and hyperplasia of PAS+ mucus-producing cells, were noticed following two 48 h interval intranasal instillations of PM\({}_{2.5}\) (1 mg/kg). These findings were validated through histomorphometrical analysis. The PM\({}_{2.5}\) control mice exhibited significant increases (\(p\) < 0.01) in mean alveolar septal thickness, secondary bronchus mucosa thickness, and increased numbers of PAS+ mucus-producing cells and infiltrating inflammatory cells in alveolar regions, along with decreases in ASA when compared to the untreated vehicle control mice. However, dose-dependent and significant (\(p\) < 0.01) improvements were observed by oral administration of AJ (400, 200, and 100 mg/kg) compared to the PM\({}_{2.5}\) control. AJ (400 mg/kg) showed favorable inhibitory activities against PM\({}_{2.5}\)-induced septal thickening and inflammation, comparable to AX (250 mg/kg; Figure 7; Table 2). Mean ASA in the PM\({}_{2.5}\) control changed by \(-\)47.85% compared to in the intact vehicle control, with changes for AX (250 mg/kg) and AJ (400, 200, and 100 mg/kg) being 64.31%, 65.75%, 55.30%, and 45.47%, respectively. Figure 6: MUC5 AC and MUC5B mRNA expression levels in lung tissue of mice with pulmonary injuries, either untreated or exposed to PM\({}_{2.5}\). Values are presented as means \(\pm\) S.D. of 10 mice. PM\({}_{2.5}\) refers to diesel particulate matter NIST 1650b; AX stands for amboxol hydrochloride; AJ indicates Attactylolis Rhizo (root of _Attractylodes japonica_ Koidz. ex. Kitam) extracts; MUC represents Mucin; DT3 is [PERSON]’s T3 test. Statistical significance is indicated as follows: \({}^{a}\)\(p\) < 0.01 compared with intact vehicle control by DT3 test; \({}^{b}\)\(p\) < 0.01 compared with PM\({}_{2.5}\) control by DT3 test. Alveolar septal thickness in the PM\({}_{2.5}\) control changed by 709.96% compared to intact vehicle control, with changes for AX (250 mg/kg) and AJ (400, 200, and 100 mg/kg) being \(-\)59.93%, \(-\)61.09%, \(-\)47.81%, and \(-\)36.40%, respectively. The secondary bronchus mucosa thickness in the PM\({}_{2.5}\) control changed by 34.19% compared to the intact vehicle control, with changes for AX (250 mg/kg) and AJ (400, 200, and 100 mg/kg) being 41.48%, 45.20%, 32.06%, and 18.44%, respectively. Inflammatory cell infiltration in the PM\({}_{2.5}\) control altered by 756.75% compared to the intact vehicle control, with changes for AX (250 mg/kg) and AJ (400, 200, and 100 mg/kg) being \(-\)63.34%, \(-\)64.71%, \(-\)53.22%, and \(-\)38.49%, respectively. PAS+ mucus-producing cell numbers in the PM\({}_{2.5}\) control changed by 71.25% compared to the intact vehicle control, with changes for AX (250 mg/kg) and AJ (400, 200, and 100 mg/kg) being 99.03%, 101.95%, 63.50%, and 37.71%, respectively. Figure 7: Illustrative histopathological profiles of the lung tissues from the left lobe of mice with pulmonary injuries, either untreated or treated with PM\({}_{2.5}\). (**A**): Intact vehicle control (mice orally administered with distilled water and given saline intranasal instillation); (**B**): PM\({}_{2.5}\) control (mice orally administered with distilled water and given PM\({}_{2.5}\) intranasal instillation); (**C**): AX\({}_{250}\) (mice orally administered with 250 mg/kg of AX and given PM\({}_{2.5}\) intranasal instillation); (**D**): AJ\({}_{400}\) (mice orally administered with 400 mg/kg of AJ orally and given PM\({}_{2.5}\) intranasal instillation); (**E**): AJ\({}_{200}\) (mice orally administered with 200 mg/kg of AJ and given PM\({}_{2.5}\) intranasal instillation); (**F**): AJ\({}_{100}\) (mice orally administered with 100 mg/kg of AJ and given PM\({}_{2.5}\) intranasal instillation). PM\({}_{2.5}\) refers to diesel particulate matter NIST 1650b; AX indicates amboxol hydrochloride; AJ stands for Altactyldis Rhizo (root of _Attactyldis japonica_ Koidz. ex.