## 4 Discussion  
Herbal medicines are gaining popularity due to their potential therapeutic efficacy and fewer side effects. For thousands of years, well-known herbal medications have been commonly given for a variety of diseases. The present research used a CS and LPS-induced COPD mouse disease model to explore the efficacy of JGT on the pathogenesis of COPD. JGT treatment considerably decreased production of proinflammatory cytokines and infiltration of inflammatory cells in lung tissue and BALF of CS and LPS-induced COPD mouse models. Treatment with JGT also markedly hindered COPD-induced increases in TGF-\(\beta\), \(\alpha\)-SMA, and MMP-9. In addition, phosphorylation of NF-\(\kappa\)B, ERK1/2, and p38 MAPKs is found to decrease following treatment of JGT. _Paenonia lactiflora Pallas and Glycyrrhiza uralensis_ Fischer comprise JGT. The major elements of JGT are monoterpene glycosides, monoterpenes, and carboxylic acids from Paenoniae Radix and triterpenes, flavanones, and flavonoid glycosides from Glycyrrhizae Radix et Rhiza [22]. In our data, quantitative determination of the concentrations of nine compounds in water extracts of JGT-albiflorin, gallic acid, liquiritin apioside, liquiritin, benzoic acid, liquiritin, benzoylpaenofilorin, glycyrrhizin, and paeoniflorin--by HPLC-PDA showed that paeoniflorin (55.292 mg/g) was the most abundant compound. Anti-inflammatory properties of JGT components have been demonstrated. _Glycyrrhiza uralensis_ [PERSON]'s roots and rhizomes have been used to cure dermatitis, peptic ulcer, and bronchitis [23]. Furthermore, it was discovered that it can reduce asthma symptoms by lowering airway hypersensitivity responses and oxidative stress [24]. _Paenonia lactiflora_ Pallas has also been shown to be effective in treating inflammatory airway disorders such as COPD and asthma [25]. Clinically, COPD is associated with chronic airway inflammation caused by inflammatory cell activity inside lung tissue. When exposed to pollutants that are breathed, such as cigarette smoke (CS), a key contributing factor to COPD, these cells become activated. CS  
Figure 8: Effects of JGT on activations of NF-\(\kappa\)B, ERK1/2, and p-38 in lung tissues, according to Western blot analysis. NC, normal control mice; COPD, CS & LPS-treated mice; RO, rofhumilast (5 mg/kg) along with CS & LPS-treated mice; JGT-100, JGT (100 mg/kg) along with CS & LPS-treated mice; JGT-200, JGT (200 mg/kg) along with CS & LPS-treated mice. Data are displayed as means \(\pm\) SEM. # \(p<0.05\) and # \(p<0.01\) compared with NC; * \(p<0.05\) and ** \(p<0.01\) compared with COPD. causes airway remodeling and permanent pathological alterations in the lungs including emphysema [26]. Because chronic inflammation persists even after stopping smoking, an unregulated and persistent inflammatory response can lead to lung tissue destruction and remodeling [27]. This chronic inflammation caused by infiltration into the lungs of inflammatory cells, which produce proinflammatory cytokines and chemokines. This study found that JGT treatment substantially reduced the increased number of inflammatory cells as well as cytokine and chemokine levels due to CS and LPS in BALF and lung tissues. The expression of several proinflammatory genes is increased as a result of the upregulation of TNF-\(\alpha\), IL-1, and IL-6 in COPD, which has been demonstrated to enhance inflammation by activating NF-\(\kappa\)B [28]. The immune system and inflammatory responses are regulated by the NF- \(\kappa\)B pathway, a transcriptional regulator [29]. The cytoplasm contains an inactive NF-\(\kappa\)B molecule bound to \(\kappa\)B. NF-\(\kappa\)B is dissociated from \(\kappa\)B and transferred to the nucleus after stimulation, where it induces the production of inflammatory cytokines and inducible enzymes [30]. A variety of cells express inflammatory cytokines and other inflammatory mediators under the control of the MAPKs signaling pathway [31].