Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Objective To evaluate the value of serum Mac-2 binding protein (M2BP) for assessment of the severity of schisto somiasis-induced liver fibrosis, so as to provide insights into non-invasive diagnosis and disease surveillance of liver fibrosis caused by schistosomiasis. Methods A total of 234 individuals with a history of Schistosoma japonicum infection were sampled from Xinhua Village, Lushan City, Jiangxi Province from 2019 to 2020, and 234 serum samples were collected from all participants. All participants received B-ultrasound examinations of the liver. Serum samples were categorized into four groups (grades 0, Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis groups) according to B-ultrasound examination results, and then, each group was randomly divided into a receiver operating characteristic (ROC) curve group and an efficacy assessment group at a ratio of 7∶3. Serum M2BP concentration was measured in four groups using the enzyme-linked immunosorbent assay (ELISA), and differences in serum M2BP concentrations were compared with analysis of variance and Spearman correlation analysis. Serum M2BP concentration was subjected to ROC curve analysis among individuals with different grades of schistosomiasis-induced liver fibrosis in the ROC curve group to determine the optimal diagnostic threshold of M2BP concentration at different fibrosis grades, and the area under the ROC curve (AUC) was calculated to evaluate the diagnostic performance. The diagnostic accuracy was verified by comparing the accordance rate and Kappa consistency test in the efficacy assessment group. Results Among 234 serum samples, there were 79 samples with grade 0 schistosomiasis-induced liver fibrosis, 87 samples with Grade Ⅰ, 46 samples with Grade Ⅱ and 22 samples with Grade Ⅲ according to the B-ultrasound examinations. The mean serum M2BP concentrations were (0.40 ± 0.31) [95% confidence interval (CI): (0.33, 0.47)], (0.64 ± 0.48) [95% CI: (0.53, 0.74)], (1.76 ± 0.58) [95% CI: (1.59, 1.93)] μg/mL and (2.56 ± 0.93) [95% CI: (2.14, 2.97)] μg/mL in the four groups, respectively (F = 150.796, P < 0.001), and the severity of schistosomiasis-induced liver fibrosis significantly positively correlated with serum M2BP concentration (rs = 0.715, P < 0. 001). The sample sizes of grades 0, Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis sera were randomly allocated as follows: 55 versus 24, 61 versus 26, 32 versus 14, and 15 versus 7 in the ROC curve and efficacy assessment groups, respectively, and the serum M2BP concentrations were (0.39 ± 0.29) μg/mL and (0.42 ± 0.36) μg/mL (F = 0.196, P > 0.05), (0.59 ± 0.47) μg/mL and (0.75 ± 0.51) μg/mL (F = 1.967, P > 0.05), (1.73 ± 0.59) μg/mL and (1.85 ± 0.57) μg/mL (F = 0.417, P > 0.05), and (2.46 ± 0.64) μg/mL and (2.76 ± 1.41) μg/mL (F = 0.491, P > 0.05), respectively. ROC curve analysis showed that the optimal diagnostic thresholds of serum M2BP concentration were 0.347 86 μg/mL (AUC = 0.635, P < 0.05), 1.188 83 μg/mL (AUC = 0.938, P < 0.000 1) and 2.021 21 μg/mL (AUC = 0.821, P < 0.000 1) for grade Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis. In addition, the accordance rates between the optimal diagnostic threshold of serum M2BP and B-ultrasound examinations for predicting grade Ⅰ, Ⅱ and Ⅲ schistosomiasis-induceed liver fibrosis were 69.23%, 85.71% and 71.43% (χ2 = 1.340, P > 0.05), and the overall Kappa consistency test showed moderate consistency [Kappa = 0.608, 95% CI: (0.428, 0.788); Z = 6.609, P < 0.000 1]. Conclusions Serum M2BP may serve as a potential biomarker for assessing moderate to advanced schistosomiasis-induced liver fibrosis; however, its diagnostic value for early-stage schistosomiasis-induced liver fibrosis remains limited.

Osteoarthritis (OA), a highly prevalent degenerative joint disease worldwide, is defined by articular cartilage degradation, abnormal bone remodeling, and persistent chronic inflammation. It severely compromises patients’ quality of life, and currently, there is no radical cure. Abnormal mechanical stress is widely regarded as a core driver of OA pathogenesis, and the exploration of mechanical signal perception and transduction mechanisms has become crucial for deciphering OA’s pathophysiological processes. Piezo1, a key mechanosensitive cation channel belonging to the Piezo protein family, has recently gained significant attention due to its pivotal role in mediating cellular responses to mechanical stimuli in joint tissues. This review systematically examines Piezo1’s expression patterns, regulatory mechanisms, and pathological functions in OA, with a particular focus on its dual roles in modulating chondrocyte homeostasis and bone metabolism disorders, while also delving into the underlying molecular signaling pathways and potential therapeutic implications. Piezo1, consisting of approximately 2 500 amino acids and forming a unique trimeric propeller-like structure, is widely expressed in chondrocytes, osteocytes, mesenchymal stem cells, and synovial cells. It exhibits permeability to cations such as Ca²⁺, K⁺, and Na⁺, and directly responds to membrane tension changes induced by mechanical stimuli like fluid shear stress and mechanical overload. In OA patients and animal models, Piezo1 expression is significantly upregulated, especially in cartilage regions subjected to abnormal mechanical stress (e.g., human temporomandibular joint cartilage). This overexpression is closely associated with aggravated cartilage degeneration, increased chondrocyte apoptosis, accelerated cellular senescence, and intensified inflammatory responses. Mechanical overload and pro-inflammatory cytokines (e.g., IL-1β) are key inducers of Piezo1 upregulation: IL-1β activates the PI3K/AKT/mTOR signaling pathway to enhance Piezo1 expression, forming a pathogenic positive feedback loop that inhibits chondrocyte autophagy, promotes apoptosis, and further accelerates joint degeneration. Mechanistically, Piezo1 mediates OA progression through multiple interconnected pathways. When activated by mechanical stress, Piezo1 triggers excessive Ca²⁺ influx, leading to endoplasmic reticulum stress (ERS) and mitochondrial dysfunction, which directly induce chondrocyte apoptosis. This process involves the activation of downstream signaling cascades such as cGAS-STING and YAP-MMP13/ADAMTS5. YAP, a transcriptional regulator, upregulates the expression of matrix metalloproteinase 13 (MMP13) and aggrecanase (ADAMTS5), thereby accelerating cartilage matrix degradation. Additionally, Piezo1-driven Ca²⁺ overload promotes the accumulation of reactive oxygen species (ROS) and upregulates senescence markers (p16 and p21), accelerating chondrocyte senescence via the p38MAPK and NF-κB pathways. Senescent chondrocytes secrete senescence-associated secretory phenotype (SASP) factors (e.g., IL-6, IL-1β), further amplifying joint inflammation. In terms of bone metabolism, Piezo1 maintains joint homeostasis by promoting the differentiation of fibrocartilage stem cells into chondrocytes and balancing bone formation and resorption through regulating the FoxC1/YAP axis and RANKL/OPG ratio. Therapeutically, targeting Piezo1 shows promising potential. Preclinical studies have demonstrated that Piezo1 inhibitors (e.g., GsMTx4) can reduce joint damage and alleviate pain in OA mice. Simultaneously, siRNA-mediated co-silencing of Piezo1 and TRPV4 (another mechanosensitive channel) decreases intracellular Ca²⁺ concentration, inhibits chondrocyte apoptosis, and promotes cartilage repair. Conditional knockout of Piezo1 using Gdf5-Cre transgenic mice alleviates cartilage degeneration in post-traumatic OA models by downregulating MMP13 and ADAMTS5 expression. Despite existing challenges, such as off-target effects of inhibitors, inefficient local drug delivery, and interindividual genetic variability, strategies like developing selective Piezo1 antagonists, optimizing targeted nanocarriers, and combining Piezo1-targeted therapy with physical therapy provide viable avenues for clinical translation. The authors propose that Piezo1 serves as a critical therapeutic target for OA, and future research should focus on deciphering its context-dependent regulatory networks, developing tissue-specific intervention strategies, and validating their efficacy and safety in clinical trials to address the unmet medical needs of OA patients.

Methods: This retrospective study analyzed 32 consecutive IDS patients who underwent UEDD surgery. Clinical features, laboratory data (erythrocyte sedimentation rate and C-reactive protein), and treatment outcomes were analyzed. Results: Definite microorganisms were identified in 27 patients (84.3%), with 24 (88.9%) meeting cure criteria. The cure rate was significantly higher in the detected pathogen group compared to the undetected pathogen group (88.9% vs. 80%; χ²=19.36, p<0.0001). Metagenomic next generation sequencing (mNGS) provided faster diagnosis (41.72±6.81 hours) compared to tissue culture (95.74±35.47 hours, p<0.05). The predominant causative pathogen was Mycobacterium tuberculosis, followed by Staphylococcus aureus. Significant improvements were observed in Visual Analog Scale pain scores, from a mean of 7.9 preoperatively to 1.06 at 1 year postoperatively. The Oswestry Disability Index revealed a similar trend, showing significant improvement (p<0.05). Conclusions UEDD is a viable alternative to traditional open surgery for managing IDS in high-risk patients. UEDD offers a dual therapeutic-diagnostic advantage during the initial admission phase, enabling simultaneous debridement, neurological decompression, and targeted biopsy in a single intervention. Compared with traditional tissue culture, mNGS enables rapid microbiological diagnosis and extensive pathogen coverage.

Objective:To investigate the mechanism of circular RNA RAD18(CircRAD18)in regulating daunorubicin(DNR)resistance in acute myeloid leukemia(AML)cells through the miR-185-5p/hepatoma-derived growth factor(HDGF)axis.Methods:Real-time fluorescence quantitative PCR and immunoblotting were applied to detect the expression of CircRAD18,miR-185-5p,and HDGF in human AML cell lines HL-60,U937,and human AML drug-resistant cell line KG1a.KG1a cells were cultured in vitro and randomly divided into control group,DNR group,DNR+negative control group,DNR+CircRAD18 knockdown group,and DNR+CircRAD18 knockdown+miR-185-5p inhibitor group.After transfection,real-time fluorescence quantitative PCR and immunoblotting were applied to detect the expression of CircRAD18,miR-185-5p,and HDGF of cells,CCK-8 method and Ki-67 immunofluorescence staining were applied to detect cell proliferation,flow cytometry was applied to detect cell apoptosis,and immunoblotting was applied to detect the expression of cell proliferation,apoptosis and drug resistance related proteins in each group.The double luciferase reporter gene experiment was applied to detect the targeting regulation of CircRAD18 on miR-185-5p,and miR-185-5p on HDGF in KG1a cells.Results:Compared with HL-60 and U937 cells,the expression of CircRAD18,and HDGF mRNA and protein in KG1 a cells increased(all P＜0.05),while miR-185-5p decreased(P＜0.05).Compared with the control group,the CircRAD18 expression,HDGF mRNA and protein expression,cell viability,proliferation rate,and PCNA,Bcl-2,BCRP,and P-gp protein expression in the DNR+CircRAD18 knockdown group decreased(all P＜0.05),while miR-185-5p expression,apoptosis rate,and Bax protein expression increased(all P＜0.05).There were no obvious changes in all indicators of cells in the DNR group compared with control group(P＞0.05).Compared with the DNR group,the CircRAD18 expression,HDGF mRNA and protein expression,cell viability,proliferation rate,PCNA,Bcl-2,BCRP,and P-gp protein expression in the DNR+CircRAD18 knockdown group decreased(all P＜0.05),while miR-185-5p expression,apoptosis rate,and Bax protein expression increased(all P＜0.05).There were no obvious changes in all indicators of cells in the DNR+negative control group compared with DNR group(P＞0.05).Compared with the DNR+CircRAD18 knockdown group,the HDGF mRNA and protein expression,cell viability,proliferation rate,PCNA,Bcl-2,BCRP,and P-gp protein expression in the DNR+CircRAD18 knockdown+miR-185-5p inhibitor group increased(all P＜0.05),while miR-185-5p expression,apoptosis rate,and Bax protein expression decreased(all P＜0.05).CircRAD18 was able to target and down-regulate the expression of miR-185-5p in KG1a cells,and miR-185-5p was able to target and down-regulate the HDGF expression.Conclusion:Knocking down CircRAD18 can reduce HDGF expression by up-regulating miR-185-5p,thereby weakening DNR resistance in AML cells,inhibiting KG1a cell proliferation under DNR treatment,and promoting apoptosis.

Objective:To investigate the clinical efficacy and underlying mechanisms of endoscopic sinus surgery(ESS)combined with budesonide nasal spray in the treatment of chronic rhinosinusitis with nasal polyps(CRSwNP),with a focus on its effects on symptom control,nasal mucosal function repair,immune regulation,and recurrence rate.Methods:A total of 110 patients with CRSwNP were randomly divided into a matched group(60 cases,receiving ESS alone)and an observation group(50 cases,receiving ESS followed by 6 months of postoperative budesonide nasal spray).The Lund-Kennedy score,Visual Analog Scale(VAS)score for symptoms,nasal mucociliary clearance rate(MTR),nasal mucosal T-cell subsets(CD4+/CD8+),inflammatory factors(TGF-β1,VEGF),serum marker(IL-3,IL-4,IL-5,IL-13,TSLP)and complications,recurrence rate(6 months and 12 months)were compared between the two groups before surgery and at 3 and 6 months postoperatively.Results:At 3 months postoperatively,the VAS scores for nasal obstruction,hyposmia,and facial pain in the observation group were lower than those in the matched group(0.76±0.21 vs 1.26±0.34,0.88±0.17 vs 1.48±0.33,0.37±0.07 vs 0.55±0.11,all P＜0.001).At 6 months postoperatively,the Lund-Kennedy score(1.34±0.31 vs 1.65±0.33)and MTR(7.53±1.67 vs 6.54±1.39 mm/min)in the observation group were superior to those in the matched group(both P＜0.05).The CD4+/CD8+ratio(1.03±0.17 vs 0.87±0.14)and TGF-β1 levels(568.33±75.48 vs 506.27±72.87 μg/L)were higher,while VEGF levels(145.95±27.94 vs 178.33±36.37 ng/L)were lower in the observation group(all P＜0.001).At 6 months after surgery,the levels of IL-4,IL-5,IL-13,and TSLP were lower than those in the matched group(P＜0.05).The complication rate(8.00％vs 16.67％)and recurrence rate(4.00％vs 18.33％)in the observation group were lower than those in the matched group(P＜0.05).Conclusion:ESS combined with budesonide can significantly alleviate CRSwNP symptoms and reduce the risk of recurrence by inhibiting Th2-type inflammatory responses,regulating T-cell immune balance,improving ciliary function,and suppressing angiogenesis.The synergistic mechanism involves the dynamic regulation of inflammatory microenvironment remodeling and mucosal repair,demonstrating significant clinical efficacy and safety.This study is the first to propose a postoperative management strategy that integrates mucosal repair,Th2 suppression,and inflammatory remodeling,filling a gap in research on postoperative immune microenvironment regulation.

The aim of this paper was to investigate the serotypes,virulence factors and drug resist-ance of clinical isolates of Pasteurella rnultocida of porcine origin in recent years.Morphological screening and polymerase chain reaction(PCR)were used to isolate and identify 119 isolates from nasal swabs and lung tissue samples sent from swine farms in Zhejiang Province from 2010 to 2024.The isolates of Pasteurella multocida were subjected to capsular polysaccharide serotyping,lipopolysaccharide serotyping,virulence factor detection and drug resistance analysis by PCR and Kirby-Bauer disc agar diffusion method(K-B).The results showed that there were 64 strains(53.7％)of A-type,54 strains(45.3％)of D-type and 1 strain(0.9％)of F-type among the capsu-lar polysaccharide serotypes,and 10 strains(8.4％)of L1-type,20 strains(16.8％)of L3-type,86 strains(72.2％)of L6-type,and 3 strains(2.6％)of undetermined type among the lipopolysaccha-ride serotypes.The amplification results of 10 virulence genes showed that the detection rate of virulence genes hgbA,higbB and fimA was over 86.0％,the detection rate of toxA was 8.4％,while the virulence gene tbpA was not detected.There were also differences in the distribution vir-ulence genes in different capsular polysaccharide serotypes.Virulence factor pfhA was detected in type A and F but not in type D.The detection rate of adhesin gene tadD in serotype A(92.2％)was significantly higher than that of type D(9.3％),and,on the contrary,the detection rate of ad-hesin gene hsf-l in serotype D(90.7％)was significantly higher than that of type A(20.3％).Drug resistance analysis revealed that Pasteurella multocida showed high susceptibility to antimi-crobial drugs such as amoxicillin,ampicillin,cephalosporins,doxycycline,fosfenicol and ciprofloxa-cin,and showed strong resistance to antimicrobial drugs such as lincomycin,cotrimoxazole,genta-micin and amikacin,and there were 54 multi-drug resistant strains(78.3％).In summary,capsular polysaccharide serotypes were dominated by type A and D,lipopolysaccharide serotypes were dom-inated by L6,the distribution of some virulence genes varied greatly among different serotypes,and the proportion of multi-resistant strains was high,which provide reference for the prevention and control of this disease.

Aim To investigate the effect of circRNF13 on oxaliplatin resistance in colorectal cancer cells and its related mechanism.Methods Cell transfection was used to overexpress circRNF13 in oxaliplatin-sensi-tive colorectal cancer cells SW620 or to inhibit cir-cRNF13 expression in oxaliplatin-resistant colorectal cancer cells SW620/OXA.Real-time quantitative fluo-rescent PCR(qRT-PCR)was used to detect the ex-pression levels of circRNF13,miR-16-5p,and mir-324-5p.Cell Count Kit 8(CCK-8)was used to meas-ure cell viability.Clonal formation experiments were used to measure clonal formation number.Western blot was used to detect CyclinD1,PCNA,Bax,Bcl-2 and cleaved caspase-3 protein expression level.Flow cy-tometry and in situ end labeling(TUNEL)were used to detect apoptosis.Dual luciferase assay was used to verify the targeting relationship between circRNF13 and miR-16-5p and mir-324-5p.Results The expression level of circRNF13 in SW620/OXA cells was signifi-cantly higher than that in SW620 cells,while the ex-pression levels of miR-16-5p and miR-324-5p were sig-nificantly lower than those in SW620 cells(P＜0.05).Overexpression of circRNF13 significantly in-creased the IC50 of oxaliplatin against SW620 cells,and inhibition of circRNF13 expression significantly decreased the IC50 of oxaliplatin against SW620/OXA cells.Overexpression of circRNF13 significantly in-creased cell viability,clonal formation number,Cy-clinD1,PCNA and Bcl-2 levels of oxaliplatin treated SW620 cells,while significantly decreased apoptosis rate,apoptosis index,Bax and cleaved caspase-3 lev-els(P＜0.05).Inhibition of circRNF13 expression significantly decreased the cell viability,clonal forma-tion number,CyclinD1,PCNA and Bcl-2 levels of ox-aliplatin treated SW620/OXA cells,while significantly increased the apoptosis rate,apoptosis index,Bax and cleaved caspase-3 levels(P＜0.05).circRNF13 tar-geted inhibition of the expression of miR-16-5p and mir-324-5p.Conclusions circRNF13 can increase oxaliplatin resistance in colorectal cancer cells,and the mechanism may be related to the targeted inhibition of circRNF13 on the expression of miR-16-5p,mir-324-5p and other miRNAs.

Aim To investigate the protective effect of liraglutide(LIRA)on acetaminophen(APAP)-in-duced hepatotoxicity at the in vivo level and to reveal the underlying mechanism.Methods Forty SPF grade male C57BL/6J mice were randomly divided into the Control,LIRA(200 μg·kg-1),APAP(500 mg·kg-1),LIRA+APAP,LIRA+APAP+3-methylade-nine(3-MA,30 mg·kg-1)groups,with eight mice in each group.The mice were administered for three con-secutive days,and the materials were taken after 24 h.The general condition and body weight of mice in each group were recorded,and liver morphology was ob-served.Serum ALT and AST levels,as well as SOD ac-tivity,MDA,and GSH content in liver homogenates,were measured using biochemical assay kits.The levels of inflammatory cytokines IL-6,TNF-α,and IL-1β in serum were detected by ELISA.Liver pathological changes were assessed by HE staining,while mitochon-drial and autophagosome structures in liver tissues were observed using transmission electron microscopy.The number of PCNA-positive cells in liver tissues was e-valuated using immunohistochemical staining.The pro-tein expression levels of LC3Ⅱ,p62,Bax,Bcl-2,PC-NA,and CyclinD1 in liver tissues were determined by Western blot.Results LIRA pretreatment can im-prove the general condition of mice with acetamino-phen-induced liver injury(AILI),reduce serum ALT and AST levels,and effectively ameliorate the appear-ance and morphology of the liver as well as the patho-logical damage to liver tissue.Simultaneously,the lev-els of inflammatory cytokines IL-6,TNF-α,and IL-1βare significantly decreased;SOD activity and GSH con-tent are significantly increased,while MDA content is significantly reduced.Transmission electron microsco-py observations reveal the presence of numerous auto-phagosomes in the cytoplasm of liver tissue.Immuno-histochemical staining results indicate a significant in-crease in the number of PCNA-positive cells.Further-more,the expression of LC3Ⅱ,Bcl-2,PCNA,and Cy-clinD1 proteins in liver tissue is significantly upregulat-ed,while the expression of p62 and Bax proteins is significantly downregulated.However,after interven-tion with the autophagy inhibitor 3-MA,the aforemen-tioned protective effects of LIRA are significantly.Conclusions LIRA pretreatment can significantly im-prove liver injury in AILI mice.Its protective mecha-nism may be related to enhancing autophagy in hepato-cytes,thereby reducing oxidative stress,inflammatory response and apoptosis in liver of AILI mice.