BACKGROUND:Curcumin is the main active ingredient of turmeric and has significant medicinal value in anti-tumor,anti-inflammatory,antioxidant and other aspects.However,its poor water solubility,unstable chemical properties and easy decomposition lead to difficulty in extracting curcumin and low extraction yield.Therefore,it is particularly important to optimize the curcumin extraction method.OBJECTIVE:To enhance the extraction yield and utilization value of curcumin and optimize the curcumin extraction process and curcumin nanoparticle preparation process.METHODS:Curcumin was extracted from turmeric by ethanol extraction,ultrasonic extraction,ionic liquid extraction,enzyme extraction,and ionic liquid combined with ultrasonic assisted enzyme extraction.The curcumin extraction yield was detected by high performance liquid chromatography;the best extraction method was determined,and subsequent process optimization experiments were carried out.The curcumin extraction yield was the response value with the type of ionic liquid,reaction temperature,ultrasonic time,liquid-to-solid ratio,ionic liquid concentration,and enzyme-drug mass ratio as parameters.The optimal production process of ionic liquid combined with ultrasonic assisted enzyme extraction was determined by single factor combined response surface experiment.The optimal process for preparing curcumin nanoparticles by ionic crosslinking method was determined by single factor combined response surface experiment with acetic acid concentration,chitosan to sodium tripolyphosphate mass ratio,stirring rate,curcumin mass concentration,sodium tripolyphosphate mass concentration,and chitosan mass concentration as parameters,and drug encapsulation efficiency as response value.Curcumin nanoparticles were prepared under the optimal process,and the particle size,polydispersity index,Zata potential value,drug loading,stability,hemolysis rate,and antioxidant capacity in vivo and in vitro of the nanoparticles were detected.RESULTS AND CONCLUSION:(1)Among the five extraction methods,the curcumin yield of ionic liquid combined with ultrasound-assisted enzyme extraction was the highest,and this method was selected as the curcumin extraction method for subsequent experiments.The results of single factor combined response surface experiment showed that the optimal process for curcumin extraction was:ionic liquid selected 1-hexyl-3-methylimidazolium chloride,reaction temperature 55 ℃,liquid-to-solid ratio 40 mL/g,ultrasound time 57 minutes,ionic liquid concentration 57％,enzyme-drug mass ratio 3.5:10,and the obtained turmeric extraction yield was 3.10％.The optimal preparation process of curcumin nanoparticles was:glacial acetic acid concentration 0.5％,chitosan and sodium tripolyphosphate mass ratio 5.0:1,stirring speed 150 r/min,curcumin mass concentration 2.23 mg/mL,sodium tripolyphosphate mass concentration 1.45 mg/mL,chitosan mass concentration 3.63 mg/mL,and the obtained drug encapsulation efficiency was 90.61％.(2)The drug loading of curcumin nanoparticles was(14.49±0.23)％,the average particle size was(76.95±1.65)nm,the polydispersity coefficient was 0.15±0.02,and the Zata potential value was(32.37±1.46)mV.The curcumin nanoparticles had good stability and blood compatibility,did not induce hemolysis,and had stronger antioxidant capacity in vivo and in vitro than free curcumin.(3)The results show that the process optimization not only solves the problems of low extraction yield,poor solubility,and low bioavailability of curcumin,but also enhances its antioxidant activity in vivo and in vitro.

BACKGROUND:Curcumin is the main active ingredient of turmeric and has significant medicinal value in anti-tumor,anti-inflammatory,antioxidant and other aspects.However,its poor water solubility,unstable chemical properties and easy decomposition lead to difficulty in extracting curcumin and low extraction yield.Therefore,it is particularly important to optimize the curcumin extraction method.OBJECTIVE:To enhance the extraction yield and utilization value of curcumin and optimize the curcumin extraction process and curcumin nanoparticle preparation process.METHODS:Curcumin was extracted from turmeric by ethanol extraction,ultrasonic extraction,ionic liquid extraction,enzyme extraction,and ionic liquid combined with ultrasonic assisted enzyme extraction.The curcumin extraction yield was detected by high performance liquid chromatography;the best extraction method was determined,and subsequent process optimization experiments were carried out.The curcumin extraction yield was the response value with the type of ionic liquid,reaction temperature,ultrasonic time,liquid-to-solid ratio,ionic liquid concentration,and enzyme-drug mass ratio as parameters.The optimal production process of ionic liquid combined with ultrasonic assisted enzyme extraction was determined by single factor combined response surface experiment.The optimal process for preparing curcumin nanoparticles by ionic crosslinking method was determined by single factor combined response surface experiment with acetic acid concentration,chitosan to sodium tripolyphosphate mass ratio,stirring rate,curcumin mass concentration,sodium tripolyphosphate mass concentration,and chitosan mass concentration as parameters,and drug encapsulation efficiency as response value.Curcumin nanoparticles were prepared under the optimal process,and the particle size,polydispersity index,Zata potential value,drug loading,stability,hemolysis rate,and antioxidant capacity in vivo and in vitro of the nanoparticles were detected.RESULTS AND CONCLUSION:(1)Among the five extraction methods,the curcumin yield of ionic liquid combined with ultrasound-assisted enzyme extraction was the highest,and this method was selected as the curcumin extraction method for subsequent experiments.The results of single factor combined response surface experiment showed that the optimal process for curcumin extraction was:ionic liquid selected 1-hexyl-3-methylimidazolium chloride,reaction temperature 55 ℃,liquid-to-solid ratio 40 mL/g,ultrasound time 57 minutes,ionic liquid concentration 57％,enzyme-drug mass ratio 3.5:10,and the obtained turmeric extraction yield was 3.10％.The optimal preparation process of curcumin nanoparticles was:glacial acetic acid concentration 0.5％,chitosan and sodium tripolyphosphate mass ratio 5.0:1,stirring speed 150 r/min,curcumin mass concentration 2.23 mg/mL,sodium tripolyphosphate mass concentration 1.45 mg/mL,chitosan mass concentration 3.63 mg/mL,and the obtained drug encapsulation efficiency was 90.61％.(2)The drug loading of curcumin nanoparticles was(14.49±0.23)％,the average particle size was(76.95±1.65)nm,the polydispersity coefficient was 0.15±0.02,and the Zata potential value was(32.37±1.46)mV.The curcumin nanoparticles had good stability and blood compatibility,did not induce hemolysis,and had stronger antioxidant capacity in vivo and in vitro than free curcumin.(3)The results show that the process optimization not only solves the problems of low extraction yield,poor solubility,and low bioavailability of curcumin,but also enhances its antioxidant activity in vivo and in vitro.

Debates persist regarding the efficacy and safety of azvudine, particularly its real-world outcomes. This study involved patients aged ≥60 years who were admitted to 25 hospitals in mainland China with confirmed SARS-CoV-2 infection between December 1, 2022, and February 28, 2023. Efficacy outcomes were all-cause mortality during hospitalization, the proportion of patients discharged with recovery, time to nucleic acid-negative conversion (T _NANC), time to symptom improvement (T _SI), and time of hospital stay (T _HS). Safety was also assessed. Among the 5884 participants identified, 1999 received azvudine, and 1999 matched controls were included after exclusion and propensity score matching. Azvudine recipients exhibited lower all-cause mortality compared with controls in the overall population (13.3% vs. 17.1%, RR, 0.78; 95% CI, 0.67-0.90; P = 0.001) and in the severe subgroup (25.7% vs. 33.7%; RR, 0.76; 95% CI, 0.66-0.88; P < 0.001). A higher proportion of patients discharged with recovery, and a shorter T _NANC were associated with azvudine recipients, especially in the severe subgroup. The incidence of adverse events in azvudine recipients was comparable to that in the control group (2.3% vs. 1.7%, P = 0.170). In conclusion, azvudine showed efficacy and safety in older patients hospitalized with COVID-19 during the SARS-CoV-2 omicron wave in China.

Objective To investigate the effect of diosgenin on the proliferation and apoptosis of breast cancer cells and its potential molecular mechanism. Methods The breast cancer cell line MCF-7 was treated with low, medium, and high doses of diosgenin, and cell proliferation was detected through the MMT method. Flow cytometry was used to detect cell apoptosis. Nuclear-cytoplasmic-protein separation method was applied to detect the subcellular localization of death associated protein (DAXX). qRT-PCR and Western blot were used to detect the expressions of DAXX and c-Jun N-terminal kinase pathway (JNK)-related proteins. Results Diosgenin considerably inhibited the proliferation of MCF-7 cells and promoted cell apoptosis in a concentration-dependent manner. Diosgenin can promote the movement of DAXX from nucleus into the cytoplasm. Diosgenin upregulated the expression of cell surface death receptor (Fas), increased the phosphorylation levels of JNK and mitogen activated protein kinase (p38), and activated the JNK/p38 signaling pathway with concentration dependence. Conclusion Diosgenin inhibits the proliferation and promotes the apoptosis of the breast cancer cell line MCF-7, whose mechanism may be related to the regulation of DAXX subcellular localization and the activation of JNK/p38 signaling pathway.

Objective To investigate the mechanism of serine protease inhibitor A3N(SerpinA3N)in alleviating reti-nal neural injury in diabetic mice by inhibiting Müller cell inflammation.Methods Thirty-six db/db mice(72 eyes)were randomly divided into the db/db group,the db/db+SerpinA3N-overexpressing adeno-associated virus(AAV-SerpinA3N)group,and the db/db+empty vector adeno-associated virus(NC-SerpinA3N)group,with 12 mice in each group.Twelve age-matched healthy male littermate mice were randomly selected as the healthy control group(db/m group).Mice in each group were sacrificed 4 weeks after the corresponding treatments.Immunofluorescence staining was used to detect the co-localization of SerpinA3N and glial fibrillary acidic protein(GFAP)in the mouse retina.Hematoxylin-eosin(HE)staining was used to observe histopathological changes in the retinal tissue.TUNEL staining was used to detect the apoptosis of reti-nal ganglion cells(RGCs).Immunohistochemistry was used to detect GFAP expression.ELISA was used to measure the levels of inflammatory factors[interleukin(IL)-1 β,IL-6,IL-18,and tumor necrosis factor-α(TNF-α)]in the retinal tis-sue.The predicted target genes of SerpinA3N were imported into the STRING database to construct a protein-protein inter-action(PPI)network.The highest-scoring target was selected based on the scores for molecular docking.Western blot was used to detect the expression levels of SerpinA3N,nuclear factor kappa B(NF-κB),and spleen focus-forming virus proviral integration oncogene(Spi1)proteins in the retinal tissue.Results Immunofluorescence staining showed co-lo-calized expression of SerpinA3N and GFAP in the retinal tissue.Compared with the db/m group,the db/db,db/db+NC-SerpinA3N,and db/db+AAV-SerpinA3N groups showed decreased retinal thickness and RGC count,and increased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and expression lev-els of NF-κB and Spi1 proteins,while SerpinA3N protein expression was decreased(all P＜0.05).Compared with the db/db group,the db/db+AAV-SerpinA3N group showed increased retinal thickness and RGC count,and decreased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and expression levels of NF-κB and Spi1 proteins,while SerpinA3N protein expression was increased(all P＜0.05).Compared with the db/db+AAV-SerpinA3N group,the db/db+NC-SerpinA3N group showed decreased retinal thickness and RGC count,and increased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and ex-pression levels of NF-κB and Spi1 proteins,while SerpinA3N protein expression was decreased(all P＜0.05).The PPI re-sults indicated an interaction between SerpinA3N and Spi1.Molecular docking results showed that Spi1 could form hydro-gen bonds with residues surrounding SerpinA3N.Conclusion Overexpression of SerpinA3N can inhibit Müller cell in-flammation and ameliorate retinal neural injury in diabetic mice,and the mechanism may be associated with the inhibition of the Spi1/NF-κB signaling pathway.

Objective To investigate the mechanism of serine protease inhibitor A3N(SerpinA3N)in alleviating reti-nal neural injury in diabetic mice by inhibiting Müller cell inflammation.Methods Thirty-six db/db mice(72 eyes)were randomly divided into the db/db group,the db/db+SerpinA3N-overexpressing adeno-associated virus(AAV-SerpinA3N)group,and the db/db+empty vector adeno-associated virus(NC-SerpinA3N)group,with 12 mice in each group.Twelve age-matched healthy male littermate mice were randomly selected as the healthy control group(db/m group).Mice in each group were sacrificed 4 weeks after the corresponding treatments.Immunofluorescence staining was used to detect the co-localization of SerpinA3N and glial fibrillary acidic protein(GFAP)in the mouse retina.Hematoxylin-eosin(HE)staining was used to observe histopathological changes in the retinal tissue.TUNEL staining was used to detect the apoptosis of reti-nal ganglion cells(RGCs).Immunohistochemistry was used to detect GFAP expression.ELISA was used to measure the levels of inflammatory factors[interleukin(IL)-1 β,IL-6,IL-18,and tumor necrosis factor-α(TNF-α)]in the retinal tis-sue.The predicted target genes of SerpinA3N were imported into the STRING database to construct a protein-protein inter-action(PPI)network.The highest-scoring target was selected based on the scores for molecular docking.Western blot was used to detect the expression levels of SerpinA3N,nuclear factor kappa B(NF-κB),and spleen focus-forming virus proviral integration oncogene(Spi1)proteins in the retinal tissue.Results Immunofluorescence staining showed co-lo-calized expression of SerpinA3N and GFAP in the retinal tissue.Compared with the db/m group,the db/db,db/db+NC-SerpinA3N,and db/db+AAV-SerpinA3N groups showed decreased retinal thickness and RGC count,and increased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and expression lev-els of NF-κB and Spi1 proteins,while SerpinA3N protein expression was decreased(all P＜0.05).Compared with the db/db group,the db/db+AAV-SerpinA3N group showed increased retinal thickness and RGC count,and decreased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and expression levels of NF-κB and Spi1 proteins,while SerpinA3N protein expression was increased(all P＜0.05).Compared with the db/db+AAV-SerpinA3N group,the db/db+NC-SerpinA3N group showed decreased retinal thickness and RGC count,and increased number of TUNEL-positive cells,relative GFAP-positive expression intensity,levels of all inflammatory factors,and ex-pression levels of NF-κB and Spi1 proteins,while SerpinA3N protein expression was decreased(all P＜0.05).The PPI re-sults indicated an interaction between SerpinA3N and Spi1.Molecular docking results showed that Spi1 could form hydro-gen bonds with residues surrounding SerpinA3N.Conclusion Overexpression of SerpinA3N can inhibit Müller cell in-flammation and ameliorate retinal neural injury in diabetic mice,and the mechanism may be associated with the inhibition of the Spi1/NF-κB signaling pathway.

OBJECTIVE To investigate the effects and potential mechanism of paeoniflorin on oxidative stress of ulcerative colitis(UC)mice based on adenosine monophosphate-activated protein kinase(AMPK)/nuclear factor-erythroid 2-related factor 2(Nrf2)pathway.METHODS Male BALB/c mice were randomly divided into control group,model group,inhibitor group(AMPK inhibitor Compound C 20 mg/kg),paeoniflorin low-,medium-and high-dose groups(paeoniflorin 12.5,25,50 mg/kg),high-dose of paeoniflorin+inhibitor group(paeoniflorin 50 mg/kg+Compound C 20 mg/kg),with 8 mice in each group.Except for the control group,mice in all other groups were given 4%dextran sulfate sodium solution for 5 days to establish the UC model.Subsequently,mice in each drug group were given the corresponding drug solution intragastrically or intraperitoneally,once a day,for 7 consecutive days.The changes in body weight of mice were recorded during the experiment.Twenty-four hours after the last administration,colon length,malondialdehyde(MDA)content,and activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)in colon tissues were measured;histopathological morphology of colon tissues,tight junctions between intestinal epithelial cells,and histopathological scoring were all observed and evaluated;the mRNA expressions of AMPK and Nrf2,as well as the protein expressions of heme oxygenase-1(HO-1),occludin and claudin-1,were all determined in colon tissue.RESULTS Compared with model group,paeoniflorin groups exhibited recovery from pathological changes such as inflammatory cell infiltration and crypt damage in the colon tissue,as well as improved tight junction damage between intestinal epithelial cells.Additionally,significant increases or upregulations were observed in body weight,colon length,activities of SOD and GSH-Px,phosphorylation level of AMPK,and protein expression of Nrf2,HO-1,occludin,claudin-1,and mRNA expressions of AMPK and Nrf2;concurrently,MDA content and histopathological scores were significantly reduced(P＜0.05 or P＜0.01).In contrast,the inhibitor group showed comparable(P＞0.05)or worse(P＜0.05 or P＜0.01)indicators compared to the model group.Conversely,the addition of AMPK inhibitor could significantly reverse the improvement of high-dose paconiflorin(P＜0.01).CONCLUSIONS Paeoniflorin can repair intestinal epithelial cell damage in mice,improve tight junctions between epithelial cells,upregulate the expression of related proteins,and promote the expression and secretion of antioxidant-promoting molecules,thereby ameliorating UC;its mechanism may be associated with activating AMPK/Nrf2 antioxidant pathway.

ObjectiveTo explore the mechanism of Huanglian Jiedutang in inhibiting the pyroptosis mediated by NOD-like receptor protein 3 （NLRP3） inflammasomes and alleviating the acute liver injury （ALI） induced by lipopolysaccharide （LPS） in the mouse model of sepsis. MethodFifty-four male C57BL/6 mice were randomized into blank， model， low- （3.08 g·kg^-1）， medium- （6.15 g·kg^-1）， and high-dose （12.30 g·kg^-1） Huanglian Jiedutang， and positive control （dexamethasone） groups （n=9）. The mice were administrated with Huanglian Jiedutang at different doses by gavage for 7 days， and then LPS （15 mg·kg^-1） was injected intraperitoneally for the modeling of sepsis. In the positive control group， dexamethasone （0.05 g·kg^-1） was injected intraperitoneally 1.5 h after modeling， and the mouse sepsis score （MSS） was recorded 12 h after modeling. The mice were sacrificed for the collection of blood and liver tissue samples. The levels of alanine transaminase （ALT） and aspartate transaminase （AST） were measured by a biochemical analyzer. The levels of tumor necrosis factor （TNF）-α， interleukin （IL）-6， IL-1β， and IL-18 in the serum were measured by enzyme-linked immunosorbent assay kits. Hematoxylin-eosin staining was used to observe the pathological changes in the liver tissue. The content of NLRP3 was observed by the immunofluorescence assay. The expression of apoptosis-associated speck-like protein containing CARD （ASC） was detected by immunohistochemistry. The protein levels of NLRP3， ASC， Caspase-1， and gasdermin D （GSDMD） in the liver tissue were determined by Western blot. Real-time quantitative polymerase chain reaction（Real-time PCR） was employed to determine the mRNA levels of GSDMD， Caspase-1， IL-1β， and IL-18. ResultCompared with the blank group， the model group showed elevated levels of ALT and AST （P<0.01） and risen levels of inflammatory cytokines in the serum （P<0.01）. In addition， the modeling resulted in edema and necrosis in the liver， and up-regulated the protein levels of GSDMD， NLRP3， ASC， and Caspase-1 （P<0.01） and the mRNA levels of GSDMD， Caspase-1， IL-1β， and IL-18 （P<0.01）. Compared with the model group， the drug intervention groups showed reduced content of inflammatory cytokines （P<0.01）， alleviated pathological damage in the liver tissue， and down-regulated protein levels of GSDMD， NLRP3， ASC， and Caspase-1 （P<0.05，P<0.01） and mRNA levels of GSDMD， Caspase-1， IL-1β， and IL-18 （P<0.05，P<0.01） in the liver tissue. ConclusionHuanglian Jiedutang can inhibit pyroptosis and reduce inflammation by inhibiting the activation of NLRP3 inflammasomes， thus demonstrating a therapeutic effect on acute liver injury in the mouse model of sepsis induced by LPS.

ObjectiveTo explore the protective mechanism of paeoniflorin on mice with ulcerative colitis （UC） through the adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR） autophagy pathway. MethodUC mouse model was established by allowing mice freely drink 4% DSS， and 56 BALB/c male mice were randomly divided into model group， AMPK inhibitor group （20 mg·kg^-1）， paeoniflorin （50 mg·kg^-1） + inhibitor （20 mg·kg^-1） group， and high dose （50 mg·kg^-1）， medium dose （25 mg·kg^-1）， and low dose （12.5 mg·kg^-1） paeoniflorin groups. After seven days of drug intervention， the protective effect of paeoniflorin on mice with UC was determined by comparing the body weight， disease activity index （DAI） changes， and Hematoxylin-eosin （HE） staining results. Enzyme linked immunosorbent assay （ELISA） was used to detect the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum of mice in each group， and immunofluorescence was utilized to detect microtubule-associated protein 1 light chain 3 （LC3） content in the colon， AMPK， mTOR proteins， and their phosphorylated proteins including p-AMPK and p-mTOR in the colon tissue were detected by Western blot， and the mRNA expression levels of AMPK， mTOR， Beclin1， LC3， and p62 were detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultCompared with the blank group， the model group showed a decrease in body mass， an increase in DAI score， and severe pathological damage to the colon. The levels of inflammatory factors including TNF-α and IL-6 increased in serum （P<0.01）， while the protein levels of LC3 and p-AMPK/AMPK were down-regulated in colon tissue， and those of p-mTOR/mTOR were up-regulated （P<0.01）. The mRNA expression levels of AMPK and LC3 were down-regulated， while the mRNA expression levels of mTOR and p62 were up-regulated （P<0.01）. Compared with the model group and the paeoniflorin + inhibitor group， the mice treated with paeoniflorin showed an increase in body mass， a decrease in DAI score， a reduction in pathological damage to colon tissue， and a reduction in the levels of inflammatory factors of TNF-α and IL-6 in serum （P<0.05）. The protein levels of LC3 and p-AMPK/AMPK in colon tissue were up-regulated， while the protein levels of p-mTOR/mTOR were down-regulated （P<0.01）. The mRNA expression levels of AMPK， Beclin1， and LC3 were up-regulated， while the mRNA expression of mTOR and p62 were down-regulated （P<0.01）. The colon tissue of the inhibitor group was severely damaged， and the trend of various indicators was completely opposite to that of the high dose paeoniflorin group. ConclusionPaeoniflorin can enhance autophagy and reduce inflammatory damage in mice with UC by activating the AMPK/mTOR signaling pathway and thus play a protective role.

Objective:To investigate the effects of sleep disorders (SD) on the radiation injury of hematopoietic stem cells (HSCs) in bone marrow (BM).Methods:Totolly 56 C57BL/6J male mice aged 6-8 weeks were enrolled in this study. They were subjected to whole body irradiation of 60Co γ-rays with doses of 5.0 and 7.5 Gy. A SD model was established using a SD device. According to the random number table method, the mice were divided into seven groups: the control group (Con group), the SD group, the mere radiation group (IR group), the group of post-irradiation SD (IR+ SD group), the group of post-irradiation SD treated with phosphate buffer solution (IR+ SD+ PBS group), the group of post-irradiation SD treated with GSK2795039 (IR+ SD+ GSK group), and the group of post-irradiation SD treated with N-acetylcysteine (IR+ SD+ NAC group), with in eight mice each group. The changes in the peripheral blood of the mice after 5.0 Gy irradiation were detected using the collected tail venous blood, and the survival rates of the mice after 7.5 Gy irradiation were observed. The changes in the density and count of bone marrow cells were observed using hematoxylin and eosin (HE) staining. The number of hematopoietic stem cells in bone marrow (LSK cells), as well as their apoptosis level and changes in cell cycle, were detected using flow cytometry. Furthermore, indicators of LSK, such as reactive oxygen species(ROS) and mitochondrial-derived reactive oxygen species (mtROS), were analyzed. Nicotinamide adenine dinucleotide phosphate (NADP+ /NADPH) and glutathione (GSSG/GSH) were detected using an enzyme microplate reader in order to observe the oxidative stress level of LSK. Furthermore, flow cytometry was employed to sort the LSK cells from the mice, and flow cytometry was used to detect the expression of NADPH oxidase 2(NOX2) and cysteinyl aspartate specific proteinnase-1(Caspase-1), and polymerase chain reaction (PCR) was used to detect the expression of inflammatory factors such as NOX1-4, interleukin 1β (IL-1β), interleukin 6 (IL-6), interleukin 18 (IL-18), and tumor necrosis factor α (TNF-α). Results:Compared to the IR group, the IR+ SD group exhibited significantly slower recovery of white blood cells (WBC) and platelets (PLT) ( t = 4.39, 6.37, P < 0.05), the bone marrow cell count decreasing from (2.14 ± 0.38) × 10 7 to (3.59 ± 0.29) × 10 7 ( t = 8.55, P < 0.05), significantly decreased proportion of G 0-phase LSK cells, significantly increased proportion of apoptotic cells ( t = 7.53, 8.21, P < 0.05), and significantly increased DCFH-DA, MitoSOX, and NADP+ /NADPH ( t = 22.99, 29.47, 3.77, P<0.05). In the case of IR, SD further promoted the activation of NOX2 and led to increases in the mRNA expression of downstream inflammatory factors such as IL-1β, IL-6, IL-18, and TNF-α ( t = 6.95, 6.01, 8.39, 4.91, 5.56, P < 0.05). Inhibition of NOX2-ROS could prevent the SD-induced aggravation of post-irradiation hematopoietic injury. This significantly reduced the apoptotic rate of LSK cells and the expression of inflammatory factors, ultimately accelerating the hematopoietic recovery of LSK cells ( t = 9.24, 3.92, P < 0.05). Conclusions:SD can aggravate the IR-induced injury of hematopoietic stem cells in bone marrow, primarily by activating the NOX2-ROS-Caspase-1 axis. This will increase the levels of intracellular inflammatory factors and ROS, promote cell apoptosis, and ultimately inhibit the hematopoietic recovery of bone marrow.