## 3 Results
### Histopathological Alterations Observed in the Lungs  
In the PM\({}_{2.5}\) control group, significant alveolar septal thickening was observed, attributed to inflammatory cell infiltration, accompanied by elevated secondary bronchial mucosal thickening and an increased abundance of PAS-positive mucus-producing cells. Furthermore, there was a noteworthy increase in the average alveolar septal and secondary bronchial mucosal thicknesses (\(p<0.01\)), as well as an augmented number of infiltrating inflammatory cells surrounding the alveoli and an increased count of PAS-positive mucus-producing cells in the secondary bronchial mucosa. Additionally, there was an associated decrease in ASA in the PM\({}_{2.5}\) control group when compared with the normal vehicle control group. Nevertheless, in all three IAP-extract-administered groups, significant increases (\(p<0.01\)) in ASA and average alveolar septum thickness were observed in a dose-dependent manner. Additionally, there was a reduction in the quantity of infiltrating inflammatory cells surrounding the alveoli. Notably, in the IAP400 group, the inhibitory activity against PM\({}_{2.5}\)-induced alveolar septum thickening, inflammatory cell infiltration, and ASA reduction was comparable to that observed in the DEXA-administered group. Furthermore, in line with the expectorant activity [16], all three IAP-extract-administered groups demonstrated significant increases (\(p<0.05\) or \(p<0.01\)) in mean thickness of the secondary bronchial mucosa and the quantity of PAS-positive mucus-producing cells in a dose-dependent manner. Contrastingly, in the DEXA-administered group, no significant changes were observed in the average thickness of the secondary bronchial mucosa and the quantity of PAS-positive mucus-producing cells when compared to the PM\({}_{2.5}\) control group (Table 6; Figure 7).  
\begin{table}
\begin{tabular}{l c c c c c} \hline \hline \multirow{2}{*}{\begin{tabular}{c} **Items** \\ **Groups** \\ \end{tabular} } & \multirow{2}{*}{\begin{tabular}{c} **Mean ASA** \\ **(\%/mm2)** \\ \end{tabular} } & \multirow{2}{*}{\begin{tabular}{c} **Mean Alveolar** \\ **Spetal Thickness** \\ **(\(\um\))** \\ \end{tabular} } & \multirow{2}{*}{\begin{tabular}{c} **Mean Thickness** \\ **of SB (\(\um\))** \\ \end{tabular} } & \multirow{2}{*}{\
\begin{tabular}{c} **Mean IF Cell** \\ **Numbers Infiltrated** \\ **in AR** \\ **(\(\times\)10 cells/mm2)** \\ \end{tabular} } & \multirow{2}{*}{
\begin{tabular}{c} **PAS-Positive** \\ **Cells on the SB** \\ **(Cells/mm2)** \\ \end{tabular} } \\ \hline Controls & & & & & \\ vehicle & 81.34 \(\pm\) 8.03 & 7.52 \(\pm\) 1.30 & 15.68 \(\pm\) 1.81 & 62.00 \(\pm\) 13.70 & 23.00 \(\pm\) 3.16 \\ PM\({}_{2.5}\) & 35.24 \(\pm\) 7.72 a & 7.25 \(\pm\) 10.07 a & 21.39 \(\pm\) 1.34 a & 732.40 \(\pm\) 140.45 a & 36.80 \(\pm\) 4.54 a \\ DEXA & 71.16 \(\pm\) 7.40 b & 21.77 \(\pm\) 4.66 ab & 21.05 \(\pm\) 2.04 a & 180.20 \(\pm\) 64.34 ab & 34.00 \(\pm\) 12.07 \\ Test substance–IAP & & & & & \\
400 mg/kg & 57.25 \(\pm\) 7.79 ab & 21.95 \(\pm\) 5.39 ab & 31.60 \(\pm\) 2.77 ab & 184.80 \(\pm\) 30.01 ab & 86.20 \(\pm\) 14.19 ab \\
200 mg/kg & 60.39 \(\pm\) 7.96 ab & 26.37 \(\pm\) 5.00 ab & 28.82 \(\pm\) 2.25 ab & 305.00 \(\pm\) 59.75 ab & 69.60 \(\pm\) 14.57 ab \\
100 mg/kg & 50.54 \(\pm\) 2.87 ab & 30.76 \(\pm\) 4.50 ab & 26.59 \(\pm\) 1.63 ab & 399.60 \(\pm\) 90.98 ab & 53.60 \(\pm\) 10.00 ac \\ \hline \hline \end{tabular}  
* Values are expressed as mean \(\pm\) SD. ASA = Alveolar surface area; AR = Alveolar region; SB = Secondary bronchial mucosa; IF = Inflammatory; PAS = Periodic acid Schiff; DT3 = Dumett’s T3. \({}^{a}p<0.01\) versus vehicle control via DT3 test. b \(p<0.01\) and c \(p<0.05\) versus PM\({}_{2.5}\) control via DT3 test.  
\end{table}
Table 6: Histomorphometric analysis of the left lobe tissue of the lungs in mice treated with the vehicle or PM\({}_{2.5}\) to assess pulmonary injury.