Tuberculosis (TB) remains a significant global health challenge, ranking second only to COVID-19 as the leading cause of death from a single infectious agent, with 1.3 million TB-related deaths reported in 2022. Treatment efficacy has been compromised by the emergence of drug-resistant strains, including rifampin-resistant TB (RR-TB), multidrug-resistant TB (MDR-TB), and extensively drug-resistant TB (XDR-TB). Although first-line drugs like isoniazid, rifampicin, pyrazinamide, and ethambutol form the cornerstone of TB therapy, the rise of resistant strains necessitates the use of second-line drugs, which often come with increased toxicity and limited accessibility. Recent advances have focused on repurposing existing compounds and developing new drugs with novel mechanisms of action. Promising agents such as second-generation bedaquiline analogs (TBAJ-587, TBAJ-876), sudapyridine (WX-081), delamanid, pretomanid, and TBI-166 (pyrifazimine) have shown efficacy against resistant Mtb strains. Innovative treatment regimens like the BPaLM protocol-combining bedaquiline, pretomanid, linezolid, and moxifloxacin-offer shorter, all-oral therapies with higher cure rates. Personalized treatment durations and dose optimizations are becoming feasible through risk stratification algorithms and pharmacokinetic/pharmacodynamic studies. Immunotherapy is emerging as a complementary strategy to enhance the host's immune response against Mtb. Agents such as vitamin D, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), statins, metformin, and biological agents like interleukins and granulocyte-macrophage colony-stimulating factor are under exploration. Additionally, cell therapies involving mesenchymal stem cells and immune effector cells present new therapeutic avenues. Despite these advancements, significant challenges remain in achieving the World Health Organization's "End TB Strategy" goals, particularly as the COVID-19 pandemic has diverted resources and attention. Ongoing research and global collaboration are crucial to develop novel therapeutic strategies, optimize treatment regimens, and ultimately reduce the global burden of TB.
Humans ; Antitubercular Agents/therapeutic use* ; COVID-19/epidemiology* ; Tuberculosis/epidemiology*

Objective:To systematically evaluate the efficacy and safety of different antifungal medications for fungal keratitis (FK).Methods:A network meta-analysis was conducted.Four databases including PubMed, Cochrane Library, Embase, Web of Science were searched.The publication period was from inception to March 16, 2023.Two researchers followed the inclusion and exclusion criteria to screen randomized controlled trial (RCT), completed the quality assessment and extracted the information.Literature quality assessment was performed using Review Manager 5.4 bias risk assessment tool, and network meta-analysis was performed using Stata 14.0 software for cure rate, healing time, visual acuity improvement and safety of different antifungal drugs for fungal keratitis.Results:A total of 14 RCTs involving 1 681 patients were finally included in this study.The network meta-analysis showed that 0.2% chlorhexidine eye drops and 5% natamycin eye drops+ oral voriconazole had better efficacy than other interventions in cure rate, and the surface under the cumulative ranking (SUCRA) were 86.1% and 63.3%, respectively.The cure rate of 1% voriconazole eye drops was lower than that of 0.2% chlorhexidine eye drops, 5% natamycin eye drops+ oral voriconazole, 0.05% chlorhexidine eye drops, 0.1% chlorhexidine eye drops, 5% natamycin eye drops+ oral ketoconazole and 5% natamycin eye drops, showing statistically significant differences (all at P<0.05).1% voriconazole eye drops and 5% natamycin eye drops+ oral voriconazole showed better efficacy than other interventions in terms of healing time (SUCRA=66.9%, 55.7%).The combination of 5% natamycin eye drops, 1% voriconazole eye drops and oral voriconazole showed a better efficacy than others in improving visual acuity and safety (SUCRA=74.8%, 79.7%).For safety, 5% natamycin eye drops was superior to 1% voriconazole eye drops and 0.2% chlorhexidine eye drops, with statistically significant differences (both at P<0.05).In addition, there may be potential publication bias in this analysis. Conclusions:0.2% chlorhexidine eye drops and 1% voriconazole eye drops are effective in the treatment of FK.The combination use of 5% natamycin eye drops, 1% voriconazole eye drops and oral voriconazole can improve visual acuity and had good safety.

Objective:To investigate the role and significance of heme oxygenase-1 (HO-1) in regulating macrophage polarization on seawater-drowning-induced acute lung injury (ALI) in mice.Methods:Raw 264.7 cells were divided into four groups. The control group was not stimulated with artificial seawater (SW), while the SW 8 h group, SW 24 h group, and SW 72 h group stimulated with artificial seawater for 8 h, 24 h, and 72 h, respectively. The morphological changes of cells were observed, the apoptosis, the contents of inducible nitric oxide synthase (iNOS), and HO-1 protein were detected. Hmox1 flox/ floxCre+ /- and Hmox1 -/- (HO-1 M-KO) mice with conditional knockout of HO-1 gene in alveolar macrophages were produced and randomly divided into HO-1 flox/flox Control group, HO-1 flox/flox SW 24 h group, HO-1 M-KO Control group, and HO-1 M-KO SW 24 h Group, with 6 mice in each group. The mouse model of seawater-drowning-induced ALI was established by placing mice in a hollow container and then immersing them in 6 cm deep and (25±2)℃ artificial seawater for 28 s. Samples were taken 24 hours after seawater drowning to carry out alveolar lavage, and then the total cell counts and protein concentrations in bronchoalveolar lavage fluid (BALF), and the pathological changes and the iNOS protein content in lung tissues were observed. Results:Abnormally shaped Raw 264.7 cells increased while the total number of Raw 264.7 cells decreased after seawater stimulation. The apoptosis rates of the control group, SW 8 h group, SW 24 h group, and SW 72 h group were increased to (5.99±0.23)%, (16.71±1.16)%, (41.80±2.50)%, and (77.84±1.59)%, respectively, with statistically significant differences ( P<0.01). The contents of HO-1 protein in the control group, SW 8 h group, SW 24 h group, and SW 72 h group were (1.07±0.06), (1.42±0.01), (2.77±0.22), and (0.99±0.10), respectively, and the contents of HO-1 protein of both SW 8 h group and SW 24 h group increased significantly ( P<0.05). The contents of iNOS protein in the cells of the control group, SW 8 h group, SW 24 h group, and SW 72 h group were (0.94±0.10), (3.44±0.32), (1.52±0.09), and (2.26±0.11), respectively, and the contents of iNOS protein of SW 8 h group, SW 24 h group, and SW 72 h group increased significantly ( P<0.05); compared with the SW 8 h group, the HO-1 protein content increased significantly, while the iNOS protein content decreased in the SW 24 h group significantly ( P<0.01). Lung tissue injury in HO-1 M-KO mice was significantly aggravated after drowning. The cavity of pulmonary alveoli collapsed and shrunk, intra-alveolar hemorrhage occurred, alveolar septum thickened, and inflammatory cell infiltration aggravated. The cell number and protein concentration in BALF significantly increased ( P<0.01), and the iNOS content in lung tissue significantly increased( P<0.01). Conclusion:HO-1 can alleviate the seawater-drowning-induced ALI in mice by inhibiting the M1 macrophage polarization.

Objective:To investigate the role and significance of heme oxygenase-1 (HO-1) in regulating macrophage polarization on seawater-drowning-induced acute lung injury (ALI) in mice.Methods:Raw 264.7 cells were divided into four groups. The control group was not stimulated with artificial seawater (SW), while the SW 8 h group, SW 24 h group, and SW 72 h group stimulated with artificial seawater for 8 h, 24 h, and 72 h, respectively. The morphological changes of cells were observed, the apoptosis, the contents of inducible nitric oxide synthase (iNOS), and HO-1 protein were detected. Hmox1 flox/ floxCre+ /- and Hmox1 -/- (HO-1 M-KO) mice with conditional knockout of HO-1 gene in alveolar macrophages were produced and randomly divided into HO-1 flox/flox Control group, HO-1 flox/flox SW 24 h group, HO-1 M-KO Control group, and HO-1 M-KO SW 24 h Group, with 6 mice in each group. The mouse model of seawater-drowning-induced ALI was established by placing mice in a hollow container and then immersing them in 6 cm deep and (25±2)℃ artificial seawater for 28 s. Samples were taken 24 hours after seawater drowning to carry out alveolar lavage, and then the total cell counts and protein concentrations in bronchoalveolar lavage fluid (BALF), and the pathological changes and the iNOS protein content in lung tissues were observed. Results:Abnormally shaped Raw 264.7 cells increased while the total number of Raw 264.7 cells decreased after seawater stimulation. The apoptosis rates of the control group, SW 8 h group, SW 24 h group, and SW 72 h group were increased to (5.99±0.23)%, (16.71±1.16)%, (41.80±2.50)%, and (77.84±1.59)%, respectively, with statistically significant differences ( P<0.01). The contents of HO-1 protein in the control group, SW 8 h group, SW 24 h group, and SW 72 h group were (1.07±0.06), (1.42±0.01), (2.77±0.22), and (0.99±0.10), respectively, and the contents of HO-1 protein of both SW 8 h group and SW 24 h group increased significantly ( P<0.05). The contents of iNOS protein in the cells of the control group, SW 8 h group, SW 24 h group, and SW 72 h group were (0.94±0.10), (3.44±0.32), (1.52±0.09), and (2.26±0.11), respectively, and the contents of iNOS protein of SW 8 h group, SW 24 h group, and SW 72 h group increased significantly ( P<0.05); compared with the SW 8 h group, the HO-1 protein content increased significantly, while the iNOS protein content decreased in the SW 24 h group significantly ( P<0.01). Lung tissue injury in HO-1 M-KO mice was significantly aggravated after drowning. The cavity of pulmonary alveoli collapsed and shrunk, intra-alveolar hemorrhage occurred, alveolar septum thickened, and inflammatory cell infiltration aggravated. The cell number and protein concentration in BALF significantly increased ( P<0.01), and the iNOS content in lung tissue significantly increased( P<0.01). Conclusion:HO-1 can alleviate the seawater-drowning-induced ALI in mice by inhibiting the M1 macrophage polarization.

Objective:To investigate the role of NF-E2-related factor 2 (Nrf2) in lung injury caused by seawater drowning in mice.Methods:A total of 48 6-8 weeks old male wild-type C57 mice were randomly divided into two groups for experiment: (1) control group, day 1 group after drowning(Day1), day 3 group after drowning(Day3) and day 7 group after drowning(Day7) to determine the time point of seawater drowning; (2) control group, seawater drowning model group(SW), dimethyl fumarate treatment group(DMF) and seawater drowning+ DMF reatment group(SW+ DMF) to determine the role of Nrf2 in lung injury in mice caused by drowning, 6 mice per group. And 12 male C57 background Nrf2 knockout mice (Nrf2 KO) at 6-8 weeks old were divided into Nrf2 KO control group and Nrf2 KO+ seawater drowning group; 6 mice in each group. Three days after the drowning model was established, we observed the gross morphology and the pathological changes of the lung tissue, calculated the wet-to-dry weight ratio of the lungs, and tested the reduced glutathione and malondialdehyde levels.Results:Seawater drowning caused alveolar space rupture, pulmonary hemorrhage and pulmonary edema in mice. Compared with the wild-type mice, knockout of Nrf2 aggravated lung injury and oxidative stress in mice caused by seawater drowning. Nrf2 agonist DMF treatment significantly improved lung injury in mice, increased the reduced glutathione content, and decreased malondialdehyde level.Conclusion:The activation of Nrf2 can relieve lung injury and oxidative stress levels in mice caused by seawater drowning, which can play an important role in reducing lung damage caused by seawater drowning.

Objective:To investigate the role of NF-E2-related factor 2 (Nrf2) in lung injury caused by seawater drowning in mice.Methods:A total of 48 6-8 weeks old male wild-type C57 mice were randomly divided into two groups for experiment: (1) control group, day 1 group after drowning(Day1), day 3 group after drowning(Day3) and day 7 group after drowning(Day7) to determine the time point of seawater drowning; (2) control group, seawater drowning model group(SW), dimethyl fumarate treatment group(DMF) and seawater drowning+ DMF reatment group(SW+ DMF) to determine the role of Nrf2 in lung injury in mice caused by drowning, 6 mice per group. And 12 male C57 background Nrf2 knockout mice (Nrf2 KO) at 6-8 weeks old were divided into Nrf2 KO control group and Nrf2 KO+ seawater drowning group; 6 mice in each group. Three days after the drowning model was established, we observed the gross morphology and the pathological changes of the lung tissue, calculated the wet-to-dry weight ratio of the lungs, and tested the reduced glutathione and malondialdehyde levels.Results:Seawater drowning caused alveolar space rupture, pulmonary hemorrhage and pulmonary edema in mice. Compared with the wild-type mice, knockout of Nrf2 aggravated lung injury and oxidative stress in mice caused by seawater drowning. Nrf2 agonist DMF treatment significantly improved lung injury in mice, increased the reduced glutathione content, and decreased malondialdehyde level.Conclusion:The activation of Nrf2 can relieve lung injury and oxidative stress levels in mice caused by seawater drowning, which can play an important role in reducing lung damage caused by seawater drowning.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.

Objective To investigate the effect of caveolin-1 scaffolding domain (CSD) peptides on heme oxygenase-1 (HO-1) activity increasing and M1/M2 phenotype polarization in rat alveolar macrophages (AMs) induced by lipopolysaccharide (LPS).Methods Bioinformatics was used to analyze the binding of full-length wild-type CSD polypeptide and 101 amino acid deleted truncated mutant CSD polypeptide (Δ101CSD) to HO-1. Primary AMs were isolated from rats, when cell fusion reached 80％, they were synchronized with serum-free medium and divided into five groups: no treatment was given to the blank control group; LPS group was treated with 100μg/L LPS for 16 hours;LPS+ hemin group was treated with 100μg/L LPS and 20μmol/L hemin for 16 hours; wild-type CSD polypeptide+ LPS+hemin group was pretreated with 10μmol/L wild-type CSD polypeptide 6 hours before LPS treatment; Δ101CSD+ LPS+hemin group was pretreated with 10μmol/L Δ101CSD polypeptide 6 hours before LPS treatment. After treatment for 16 hours, the co-localization between caveolin-1 (Cav-1) and HO-1 was displayed by confocal microscope; the mRNA expressions of inflammatory cytokines interleukin-1β (IL-1β) and monocyte chemoattractant protein-1 (MCP-1) and M1/M2 polarization cytokines tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), leukocyte differentiation antigen 206 (CD206) and IL-10 were determined by real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-qPCR); the HO-1 activity and nitric oxide (NO) production were determined by spectrophotometry.Results Bioinformatics analysis showed: both wild-type CSD and Δ101CSD peptides could bind to HO-1, and there was no significant difference in the binding ability between the two peptides, but the deletion of 101 Arg resulted in the disappearance of part of the binding region between Δ101CSD and HO-1. The results of laser confocal microscopy showed: the expressions of Cav-1 and HO-1 were lowed in the blank control group, and Cav-1 was bound to HO-1 in LPS group and LPS+ hemin group. Both wild-type CSD and Δ101CSD peptides pretreatment could significantly reduce the binding of HO-1 to Cav-1 induced by LPS. HO-1 activity analysis showed: after LPS stimulation, the activity of HO-1 was significantly higher than that of the blank control group; the activity of HO-1 induced by LPS was increased by hemin; after pretreatment with two kinds of CSD peptides, the activity of HO-1 was further increased, and the effect of wild-type CSD peptide was more significant, which showed a statistically significant difference as compared with that of LPS+ hemin group (pmol·mg-1·h-1: 3683±266 vs. 2408±132,P < 0.05). RT-qPCR results showed: LPS could induce elevation of cytokines and M1 markers and decrease of M2 markers, while hemin could inhibit LPS-induced inflammatory response and M1/M2 phenotypic polarization. Compared with LPS+ hemin group, after pretreatment with wild-type CSD peptide, the levels of inflammatory factors in AMs were decreased, and the mRNA expression levels of TNF-α and iNOS, M1 markers, were decreased [TNF-α mRNA (2-??Ct): 6.82±0.05 vs. 8.70±0.24, iNOS mRNA (2-??Ct): 331.50±32.05 vs. 506.70±0.10, bothP < 0.05], and IL-10 mRNA expression level was increased (2-??Ct: 269.09±6.54 vs. 119.05±3.30,P < 0.05). The deletion of 101 site partially weakened the inhibitory effect of CSD peptides on inflammatory factors and only reduced the expression of iNOS mRNA (2-??Ct: 429.11±8.92 vs. 506.70±0.10,P < 0.05), indicating that its ability to transform AMs from M1 phenotype to M2 phenotype was poor. The two peptides had no effect on the expression of CD206.Conclusion Wild-type CSD had beneficial effects of anti-inflammation by reducing Cav-1 binding to HO-1 induced by LPS, restoring the HO-1 activity and driving M2 phenotype in alveolar macrophages.

Objective To evaluate the effect of methylene blue (MB) on hydrogen peroxide (H2O2)-induced apoptosis in macrophages through mitochondria-dependent pathway in mice.Methods Mouse peritoneal macrophage line RAW264.7 cells were cultured in DMEM culture medium containing 10％ fetal bovine serum.Cells were divided into 6 groups (n =24 each) using a random number table method:control group (group C),H2O2 group,prophylactic different concentrations of MB groups (MB1,2 groups) and therapeutic different concentrations of MB groups (MB3.4 groups).H2O2 50 μmol/L was added to the culture medium in group H2O2.MB was added to the culture medium with the final concentrations of 0.1 μmol/L (in MB1 and MB3 groups) and 1.0 μmol/L (in MB2 and MB4 groups) at 30 min before adding H2O2 in MB1.2 groups and 30 min after adding H2O2 in MB3.4 groups.At 24 h of culture or incubation in each group,the cell survival rate was measured by methyl thiazolyl tetrazolium assay,the activity of reactive oxygen species (ROS) in cells was determined with the fluorescent probe,the lactate dehydrogenase (LDH) activity in supernatant was detected by spectrophotometry,the activity of superoxide dismutase (SOD) in cells was detected by colorimetric method,mitochondrial membrane potential (MMP) was measured using rhodamine 123 staining,the content of ATP was determined by an ATP bioluminescent method,the expression of pro-caspase-3 and spliceosomes P20 protein and P 18 protein was detected by Western blot,and cell apoptosis was detected using flow cytometry.Results Compared with group C,the cell survival rate,SOD activity and contents of MMP and ATP were significantly decreased,the ROS activity and activity of LDH in supernatant were increased,the expression of pro-caspase-3 and spliceosomes P20 protein and P18 protein was up-regulated,and early and late apoptosis rates were increased in the other five groups (P＜0.05).Compared with group H2O2,the cell survival rate,SOD activity and contents of MMP and ATP were significantly increased,the ROS activity and activity of LDH in supernatant were decreased,the expression of pro-caspase-3 and spliceosomes P20 protein and P18 protein was down-regulated,and early and late apoptosis rates were decreased in MB1-4 groups (P＜0.05).Compared with group MB1,the cell survival rate was significantly decreased,and the expression of caspase-3 spliceosome P 18 was down-regulated in group MB2,and the cell survival rate and SOD activity were significantly decreased,and the activity of ROS was increased in group MB3 (P＜0.05).Compared with group MB4,the expression of caspase-3 spliceosome P 18 was significantly down-regulated,early and late apoptosis rates were decreased,and the activity of ROS was increased in group MB2,and the activity of ROS was significantly increased in group MB3 (P＜0.05).Conclusion The mechanism by which MB attenuates H2O2-induced oxidative damage to macrophages is related to inhibiting cell apoptosis in macrophages through mitochondria-dependent pathway in mice.