Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Objective:To assess the application value of one-hour post-load glucose (1hPG) for detecting prediabetes among individuals with high risk of type 2 diabetes mellitus (T2DM).Methods:The study was conducted between August 2023 and January 2024, and individuals with a high risk of T2DM were invited to receive an oral glucose tolerance test (OGTT), structural questionnaires, physical measurements, and other biochemical examinations. The fasting, one-, and two-hour glucose and insulin were tested. According to the 1hPG cut point on hyperglycemia suggested by International Diabetes Federation (IDF), normal glucose tolerance (NGT) and prediabetes were further divided into two subgroups, respectively, i.e., NGT with 1hPG<8.6 mmol/L (NGT-1hPG-normal), NGT with 1hPG≥8.6 mmol/L (NGT-1hPG-high), prediabetes with 1hPG<8.6 mmol/L (PDM-1hPG-normal), and prediabetes with 1hPG≥8.6 mmol/L (PDM-1hPG-high). The insulin release curve was drawn by the groups as above. Insulin resistance was evaluated by homeostasis model assessment for insulin resistance (HOMA-IR), and β-cell secretory function was evaluated by homeostasis model assessment for β cell function (HOMA-β)/HOMA-IR. Spearman rank correlation analysis was used to calculate the correlation coefficients among 1hPG, 2hPG and HOMA indices, and Steiger′s Z test was used to compare the difference between two correlation coefficients. Receiver operating characteristics (ROC) curves and area under the curve (AUC) were used to assess the accuracy of 1hPG for detecting prediabetes. Results:A total of 2 469 subjects consisting of 1 485 men (60.1%) and 984 (39.9%) women, with a mean age of (45.76±6.20) years, of which 1 844 (74.7%) had 1hPG≥8.6 mmol/L. The prevalence of 1hPG≥8.6 mmol/L was 46.8%, 93.0% and 99.8% in individuals with NGT, prediabetes and newly diagnosed T2DM, respectively ( χ 2=763.78, P<0.001). The insulin release curve showed that insulin secretion increased rapidly in subjects with NGT-1hPG-high, and peaked at one hour, then decreased rapidly, with a significantly higher level of one- and two-hour insulin than those with NGT-1hPG-normal ( P<0.001). Compared to individuals with NGT-1hPG-normal, the counterparts with NGT-1hPG-high exhibited higher HOMA-IR and lower adjusted HOMA-β ( P<0.001). Spearman rank correlation analysis showed that the correlation coefficient of 1hPG with HOMA-IR was similar to the correlation coefficient of 2hPG with HOMA-IR (0.493 vs. 0.480, P=0.550), while the correlation of 1hPG with adjusted HOMA-β was significantly stronger than that of 2hPG (-0.692 vs. -0.587, P<0.001). Excluding patients with T2DM, according to the cut point recommended by IDF, the AUC of 1hPG≥8.6 mmol/L for detecting prediabetes was 0.731 (95% CI: 0.714-0.748), and the sensitivity and specificity were 0.930 and 0.532, respectively, with the kappa value of 0.45. Conclusion:1hPG is closely related to insulin resistance and islet function, and there′s substantial value for individuals with a high risk of T2DM to detect prediabetes by using the 1hPG cut points recommended by IDF.

Objective:To investigate the inhibitory effect of Huqizhengxiao decoction (HQZXD) on subcutaneous tumor in H22 hepatoma-bearing mice and its potential mechanism.Methods:Twenty-five healthy male BALB/c inbred mice aged 4 to 6 weeks and weighing (20±2) g were taken. One of them was used for the amplification of H22 hepatoma cells. The amplified H22 hepatoma cells were inoculated subcutaneously at the left posterior axillary line of the remaining mice for modeling. After subcutaneous tumor formation, the mice were randomly divided into four groups: model group, HQZXD group, sorafenib group and combined (HQZXD+ sorafenib) group, with 6 mice in each group. Tumor inhibition rates, and serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) were observed. The expression of interleukin (IL)-6, signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in tumor tissues was detected using immunohistochemistry and Western blotting. Enzyme-linked immunosorbent assay was used to quantify the levels of IL-6, tumor necrosis factor-alpha (TNF-α), and IL-1β in tumor tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess the mRNA levels of IL-6, STAT3, and C-X-C motif chemokine ligand 1 (CXCL1) in tumor tissues.Results:The general condition of mice in all treatment groups improved compared to the model group. Notably, the tumor weight (0.50±0.22) g and tumor volume (0.37±0.18) cm 3 in the combined group were significantly lower than those in the model group [tumor weight: (1.63±0.26) g, tumor volume: (0.98±0.83) cm 3] with statistical significance (both P<0.05). The tumor inhibition rates for the sorafenib, HQZXD, and combination groups were 35.4%, 48.6%, and 69.7%, respectively. Compared to the model group, serum levels of AST and ALT were reduced in all treatment groups, with the combined group showing the most significant decrease [AST: (48.81±2.82) U/L vs. (188.12±6.51) U/L; ALT: (34.14±1.25) U/L vs. (116.62±4.72) U/L], and the differences were statistically significant (both P<0.05). The protein expression levels of IL-6, STAT3, p-STAT3, IL-1β, TNF-α, and NLRP3 in tumor tissues were reduced in all treatment groups compared to the model group, with the combined group showing the most marked reduction, and the differences were statistically significant (all P<0.05). Similarly, the mRNA levels of IL-6, STAT3, and CXCL1 in tumor tissues were lower in all treatment groups compared to the model group, with the combined group showing lower levels than the single treatment groups, and these differences were statistically significant (all P<0.05). Conclusion:HQZXD can inhibit the activation of IL-6/STAT3 pathway, reduce inflammation in tumors, and consequently play a certain inhibitory effect on tumor.

Objective:To assess the application value of one-hour post-load glucose (1hPG) for detecting prediabetes among individuals with high risk of type 2 diabetes mellitus (T2DM).Methods:The study was conducted between August 2023 and January 2024, and individuals with a high risk of T2DM were invited to receive an oral glucose tolerance test (OGTT), structural questionnaires, physical measurements, and other biochemical examinations. The fasting, one-, and two-hour glucose and insulin were tested. According to the 1hPG cut point on hyperglycemia suggested by International Diabetes Federation (IDF), normal glucose tolerance (NGT) and prediabetes were further divided into two subgroups, respectively, i.e., NGT with 1hPG<8.6 mmol/L (NGT-1hPG-normal), NGT with 1hPG≥8.6 mmol/L (NGT-1hPG-high), prediabetes with 1hPG<8.6 mmol/L (PDM-1hPG-normal), and prediabetes with 1hPG≥8.6 mmol/L (PDM-1hPG-high). The insulin release curve was drawn by the groups as above. Insulin resistance was evaluated by homeostasis model assessment for insulin resistance (HOMA-IR), and β-cell secretory function was evaluated by homeostasis model assessment for β cell function (HOMA-β)/HOMA-IR. Spearman rank correlation analysis was used to calculate the correlation coefficients among 1hPG, 2hPG and HOMA indices, and Steiger′s Z test was used to compare the difference between two correlation coefficients. Receiver operating characteristics (ROC) curves and area under the curve (AUC) were used to assess the accuracy of 1hPG for detecting prediabetes. Results:A total of 2 469 subjects consisting of 1 485 men (60.1%) and 984 (39.9%) women, with a mean age of (45.76±6.20) years, of which 1 844 (74.7%) had 1hPG≥8.6 mmol/L. The prevalence of 1hPG≥8.6 mmol/L was 46.8%, 93.0% and 99.8% in individuals with NGT, prediabetes and newly diagnosed T2DM, respectively ( χ 2=763.78, P<0.001). The insulin release curve showed that insulin secretion increased rapidly in subjects with NGT-1hPG-high, and peaked at one hour, then decreased rapidly, with a significantly higher level of one- and two-hour insulin than those with NGT-1hPG-normal ( P<0.001). Compared to individuals with NGT-1hPG-normal, the counterparts with NGT-1hPG-high exhibited higher HOMA-IR and lower adjusted HOMA-β ( P<0.001). Spearman rank correlation analysis showed that the correlation coefficient of 1hPG with HOMA-IR was similar to the correlation coefficient of 2hPG with HOMA-IR (0.493 vs. 0.480, P=0.550), while the correlation of 1hPG with adjusted HOMA-β was significantly stronger than that of 2hPG (-0.692 vs. -0.587, P<0.001). Excluding patients with T2DM, according to the cut point recommended by IDF, the AUC of 1hPG≥8.6 mmol/L for detecting prediabetes was 0.731 (95% CI: 0.714-0.748), and the sensitivity and specificity were 0.930 and 0.532, respectively, with the kappa value of 0.45. Conclusion:1hPG is closely related to insulin resistance and islet function, and there′s substantial value for individuals with a high risk of T2DM to detect prediabetes by using the 1hPG cut points recommended by IDF.

Objective:To investigate the inhibitory effect of Huqizhengxiao decoction (HQZXD) on subcutaneous tumor in H22 hepatoma-bearing mice and its potential mechanism.Methods:Twenty-five healthy male BALB/c inbred mice aged 4 to 6 weeks and weighing (20±2) g were taken. One of them was used for the amplification of H22 hepatoma cells. The amplified H22 hepatoma cells were inoculated subcutaneously at the left posterior axillary line of the remaining mice for modeling. After subcutaneous tumor formation, the mice were randomly divided into four groups: model group, HQZXD group, sorafenib group and combined (HQZXD+ sorafenib) group, with 6 mice in each group. Tumor inhibition rates, and serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) were observed. The expression of interleukin (IL)-6, signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in tumor tissues was detected using immunohistochemistry and Western blotting. Enzyme-linked immunosorbent assay was used to quantify the levels of IL-6, tumor necrosis factor-alpha (TNF-α), and IL-1β in tumor tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess the mRNA levels of IL-6, STAT3, and C-X-C motif chemokine ligand 1 (CXCL1) in tumor tissues.Results:The general condition of mice in all treatment groups improved compared to the model group. Notably, the tumor weight (0.50±0.22) g and tumor volume (0.37±0.18) cm 3 in the combined group were significantly lower than those in the model group [tumor weight: (1.63±0.26) g, tumor volume: (0.98±0.83) cm 3] with statistical significance (both P<0.05). The tumor inhibition rates for the sorafenib, HQZXD, and combination groups were 35.4%, 48.6%, and 69.7%, respectively. Compared to the model group, serum levels of AST and ALT were reduced in all treatment groups, with the combined group showing the most significant decrease [AST: (48.81±2.82) U/L vs. (188.12±6.51) U/L; ALT: (34.14±1.25) U/L vs. (116.62±4.72) U/L], and the differences were statistically significant (both P<0.05). The protein expression levels of IL-6, STAT3, p-STAT3, IL-1β, TNF-α, and NLRP3 in tumor tissues were reduced in all treatment groups compared to the model group, with the combined group showing the most marked reduction, and the differences were statistically significant (all P<0.05). Similarly, the mRNA levels of IL-6, STAT3, and CXCL1 in tumor tissues were lower in all treatment groups compared to the model group, with the combined group showing lower levels than the single treatment groups, and these differences were statistically significant (all P<0.05). Conclusion:HQZXD can inhibit the activation of IL-6/STAT3 pathway, reduce inflammation in tumors, and consequently play a certain inhibitory effect on tumor.

Objective To investigate the mechanism and clinical significance of miR-18a-5p and retinoid acid receptor-related orphan receptor-α(RORA)in the proliferation and progression of colorectal cancer(CRC)cells.Methods The expressions of miR-18a-5p and RORA in CRC cells and tissues were detected via qRT-PCR,FISH,and IHC.Cell proliferation capability was detected through EdU and CFSE assay,cell apoptosis by flow cytometry assay,and cell migration and invasion abilities by cell scratch and Transwell invasion assays,respectively.The targeted regulation of miR-18a-5p on RORA was further verified via dual-luciferase reporter assay,cell function rescue test,RT-PCR,and Western blot assay.Finally,bioinformatics was used to explore the molecular mechanism of miR-18a-5p promoting malignant proliferation,invasion,and progression of CRC via regulating RORA.Results miR-18a-5p exhibited a high expression in CRC tissues and cells(P<0.05)and promoted the proliferation,migration,and invasion of CRC cells(P<0.05).In addition,RORA served as the target gene of miR-18a-5p,and its overexpression effectively reduced the promoting function of miR-18a-5p in the malignant biological phenotype of CRC cells(P<0.05).The expression of RORA in CRC tissues showed a significantly positively correlation with the infiltration of CD8+T cells and the expression of its surface marker protein CD8A.Conclusion The targeted regulation of RORA by miR-18a-5p promotes the proliferation and progression of CRC.The miR-18a-5p/RORA regulatory pathway possibly contributes to the immune microenvironment of CRC,which can be a potential therapeutic target for CRC.

Objective To investigate the effect of Fuzheng Touxie Jiedu Decoction on lung injury in Pseudomonas aeruginosa pneumonia(PAP)rats and explore its possible mechanism.Methods The suspension of Pseudomonas aeruginosa(3×109 CFU/mL)0.1 mL was injected by orotracheal cannula to replicate the PAP rat model.A total of 36 SD rats were divided into the normal group,the model group,the Fuzheng Touxie Jiedu Decoction low-(3.18 g/kg),medium-(6.36 g/kg),high-(12.72 g/kg)dose groups and the piperacillin group(0.27g/kg)according to random number table method,with six rats in each group.Rats in each drug administration group received the corresponding drugs,while rats in the normal and model groups received an equal volume of distilled water by gavage once a day for seven consecutive days.Nucleic acid values of Pseudomonas aeruginosa were detected in the lung tissues of rats in each group by real-time fluorescence PCR.Hematoxylin-eosin staining was used to observe pathological morphological changes in lung tissues in rats in each group.Flow cytometry assay was used to detect the differentiation of T helper 17(Th17)cells and regulatory T(Treg)cells in the peripheral blood of rats in each group.Serum tumor necrosis factor-α(TNF-α),transforming growth factor-β(TGF-β),interleukin-6(IL-6),interleukin-10(IL-10),and interleukin-17(IL-17)levels were detected in rats of each group with an enzyme-linked immunosorbent assay.The mRNA level of retinoid-related orphan receptor γt(RORγt),forkhead box protein 3(FoxP3),and related inflammatory factors were detected by real-time fluorescence PCR.The protein expressions of RORγt,FoxP3,and related inflammatory factors were detected by Western blotting.Results The positive detection of Pseudomonas aeruginosa in the serum of model rats and the obvious inflammatory lesions observed in the pathological tissue sections indicated successful modeling.A large number of inflammatory cell infiltration,structural damage and epithelial cell shedding were observed in the lung issue of the model group rats.Compared to the normal group,the proportion of Th17 in CD4 T+cells of peripheral blood of rats in the model group increased,the proportion of Treg decreased and the ratio of Th17/Treg increased(P<0.01).The contents of TNF-α,TGF-β,IL-6,and IL-17 in serum were increased,while IL-10 was decreased(P<0.01).The mRNA expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 increased,while the mRNA expression levels of FoxP3 and IL-10 decreased in the model group(P<0.01).The protein expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were increased,while those of FoxP3 and IL-10 were decreased(P<0.05,P<0.01).Compared to the model group,damage to lung structure,epithelial exfoliation condition,and inflammatory cell infiltration improved in the Fuzheng Touxie Jiedu Decoction low-,medium-,and high-dose groups and the piperacillin group.The proportion of Th17 decreased,the proportion of Treg increased,and the ratio of Th17/Treg decreased(P<0.05,P<0.01)in the Fuzheng Touxie Jiedu Decoction medium-and high-dose groups and the piperacillin group.Serum levels of TNF-α,TGF-β,IL-6,and IL-17 decreased,while anti-inflammatory factor(IL-10)levels increased in rats in all drug-administered groups(P<0.05,P<0.01).The mRNA expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were decreased,the mRNA expression levels of FoxP3 and IL-10 were increased in the Fuzheng Touxie Jiedu Decoction medium-,high-dose groups and the piperacillin group(P<0.05,P<0.01).The protein expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were decreased,the protein expression levels of FoxP3 and IL-10 were increased in the Fuzheng Touxie Jiedu Decoction medium-,high-dose groups and the piperacillin groups(P<0.01).Conclusion Fuzheng Touxie Jiedu Decoction showed a remarkable capability to alleviate lung inflammatory injury in PAP rat models,reduce the levels of proinflammatory factors,and enhance anti-inflammatory factors.Therapeutic efficacy is believed to operate through regulation of Th17/Treg immune balance.

Objective To investigate the effect of Fuzheng Touxie Jiedu Decoction on lung injury in Pseudomonas aeruginosa pneumonia(PAP)rats and explore its possible mechanism.Methods The suspension of Pseudomonas aeruginosa(3×109 CFU/mL)0.1 mL was injected by orotracheal cannula to replicate the PAP rat model.A total of 36 SD rats were divided into the normal group,the model group,the Fuzheng Touxie Jiedu Decoction low-(3.18 g/kg),medium-(6.36 g/kg),high-(12.72 g/kg)dose groups and the piperacillin group(0.27g/kg)according to random number table method,with six rats in each group.Rats in each drug administration group received the corresponding drugs,while rats in the normal and model groups received an equal volume of distilled water by gavage once a day for seven consecutive days.Nucleic acid values of Pseudomonas aeruginosa were detected in the lung tissues of rats in each group by real-time fluorescence PCR.Hematoxylin-eosin staining was used to observe pathological morphological changes in lung tissues in rats in each group.Flow cytometry assay was used to detect the differentiation of T helper 17(Th17)cells and regulatory T(Treg)cells in the peripheral blood of rats in each group.Serum tumor necrosis factor-α(TNF-α),transforming growth factor-β(TGF-β),interleukin-6(IL-6),interleukin-10(IL-10),and interleukin-17(IL-17)levels were detected in rats of each group with an enzyme-linked immunosorbent assay.The mRNA level of retinoid-related orphan receptor γt(RORγt),forkhead box protein 3(FoxP3),and related inflammatory factors were detected by real-time fluorescence PCR.The protein expressions of RORγt,FoxP3,and related inflammatory factors were detected by Western blotting.Results The positive detection of Pseudomonas aeruginosa in the serum of model rats and the obvious inflammatory lesions observed in the pathological tissue sections indicated successful modeling.A large number of inflammatory cell infiltration,structural damage and epithelial cell shedding were observed in the lung issue of the model group rats.Compared to the normal group,the proportion of Th17 in CD4 T+cells of peripheral blood of rats in the model group increased,the proportion of Treg decreased and the ratio of Th17/Treg increased(P<0.01).The contents of TNF-α,TGF-β,IL-6,and IL-17 in serum were increased,while IL-10 was decreased(P<0.01).The mRNA expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 increased,while the mRNA expression levels of FoxP3 and IL-10 decreased in the model group(P<0.01).The protein expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were increased,while those of FoxP3 and IL-10 were decreased(P<0.05,P<0.01).Compared to the model group,damage to lung structure,epithelial exfoliation condition,and inflammatory cell infiltration improved in the Fuzheng Touxie Jiedu Decoction low-,medium-,and high-dose groups and the piperacillin group.The proportion of Th17 decreased,the proportion of Treg increased,and the ratio of Th17/Treg decreased(P<0.05,P<0.01)in the Fuzheng Touxie Jiedu Decoction medium-and high-dose groups and the piperacillin group.Serum levels of TNF-α,TGF-β,IL-6,and IL-17 decreased,while anti-inflammatory factor(IL-10)levels increased in rats in all drug-administered groups(P<0.05,P<0.01).The mRNA expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were decreased,the mRNA expression levels of FoxP3 and IL-10 were increased in the Fuzheng Touxie Jiedu Decoction medium-,high-dose groups and the piperacillin group(P<0.05,P<0.01).The protein expression levels of RORγt,TNF-α,TGF-β,IL-6,and IL-17 were decreased,the protein expression levels of FoxP3 and IL-10 were increased in the Fuzheng Touxie Jiedu Decoction medium-,high-dose groups and the piperacillin groups(P<0.01).Conclusion Fuzheng Touxie Jiedu Decoction showed a remarkable capability to alleviate lung inflammatory injury in PAP rat models,reduce the levels of proinflammatory factors,and enhance anti-inflammatory factors.Therapeutic efficacy is believed to operate through regulation of Th17/Treg immune balance.