To investigate the effect of arctigenin on bronchial epithelial cell injury caused by Pseudomonas aeruginosa (PA) infection and its mechanism.

BEAS-2B cells were randomly divided into control group (conventional culture), PA group (1.50×10⁸ CFU·mL^-1 PA infection), PA+ low dose group (PA combined with 10.00 mmol·L^-1 burdock aglycone), PA+ high-dose group (PA combined with 20.00 mmol·L^-1 burdock aglycone). The expression of inflammatory factors and glutathione (GSH) was detected by kit assay, glutathione peroxidase 4 (GPX4) protein was detected by Western blot assay, and lipid peroxidation levels were detected by immunofluorescence assay.

The IL-6 contents of control group, PA group, PA+ low dose group and PA+ high dose group were (20.43±2.82), (106.28±8.07), (76.66±5.73) and (50.57±3.98) pg·mL^-1, respectively; the GSH contents were (25.95±1.46), (10.59±0.60), (13.98±0.74) and (21.52±2.36) ng·mL^-1, respectively; GPX4 protein expression levels were 0.76±0.06, 0.33±0.05, 0.46±0.05 and 0.62±0.06, respectively; the lipid peroxidation levels were (100.00±4.29)%, (470.91±36.33)%, (331.16±27.04)% and (160.16±18.65)%, respectively. The above indexes in PA group compared with control group, PA+ low dose group and PA+ high dose group were compared with PA group, and the differences were all statistically significant (all P<0.01).

Arctigenin can reduce the inflammation of PA-infected BEAS-2B cells by inhibiting GPX4-related ferroptosis pathway.

To explore the effect and mechanism of circular RNA RAS p21 protein activator 2 (circRASA2) mediated by nobiletin (NOB) on lipopolysaccharide (LPS)-induced hPDLCs in periodontal ligament cells.

hPDLCs cells were divided into control group, model group (hPDLCs cells were treated with 10 μg·mL^-1 LPS for 24 h), NOB-H group (Based on the model group, 20 μmol·L^-1 NOB was given for 24 h), NOB+oe-NC group (hPDLCs cells transfected with oe-NC were treated with 20 μmol·L^-1 NOB) and NOB+oe-circRASA2 group (hPDLCs cells transfected with oe-circRASA2 were treated with 20 μmol·L^-1 NOB). Quantitative real time polymerase chain reaction was used to detect the mRNA expression levels of circRASA2. The secretion levels of inflammation-related factors were detected by enzyme-linked immunosorbent assay. Western blot analysis of slit homolog 2 (Slit2)/mitogen-activated protein kinase (MAPK) signaling pathway related protein expression levels.

The relative expression levels of circRASA2 in control group, model group and NOB-H group were 1.00±0.15, 2.83±0.50 and 1.36±0.27, respectively. The levels of interleukin-1β in control group, model group, NOB-H group, NOB+oe-NC group and NOB+oe-circRASA2 group were (144.82±24.89), (367.54±65.73), (228.51±40.24), (219.78±36.94) and (324.25±61.57) mg·mL^-1, respectively; interleukin-18 levels were (167.50±27.33), (394.68±74.96), (212.47±39.51), (205.93±41.18) and (358.11±66.27) mg·mL^-1, respectively; the relative expression levels of Slit2 protein were 1.00±0.18, 2.35±0.41, 1.61±0.29, 1.57±0.27 and 2.14±0.38, respectively; the ratios of phospho-p38 mitogen-activated protein kinase/p38 mitogen-activated protein kinase protein were 1.00±0.16, 2.08±0.37, 1.39±0.25, 1.33±0.21 and 1.92±0.34, respectively. The above indexes in the model group were compared with the control group, the NOB-H group was compared with the model group, and the NOB+oe-circRASA2 group was compared with the NOB+oe-NC group, and the differences were statistically significant (all P<0.05).

NOB alleviates LPS-induced inflammation and inhibits pyroptosis in hPDLCs cells by inhibiting circRASA2 expression, possibly by inhibiting Slit2/MAPK signaling pathway.

To investigate the effect of anemoside B4 on the malignant biological behavior of non-small cell lung cancer (NSCLC) cells mediated by microRNA-142-3p (miR-142-3p) on the expression of high mobility group protein A1 (HMGA1).

A549 cells were divided into A549 group (normal culture), anemoside B4 group (100 μg·mL^-1 anemoside B4 treatment), inhibitor NC group (100 μg·mL^-1 anemoside B4+ transfection inhibitor NC treatment), miR-142-3p inhibitor group (100 μg·mL^-1 anemoside B4+ transfected with miR-142-3p inhibitor treatment), si-NC group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-NC treatment), si-HMGA1 group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-HMGA1 treatment). Real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to detect the expression of miR-142-3p and HMGA1. Cell proliferation, migration and apoptosis were detected by 5-acetylidene-2′-deoxyuracil riboside (Edu), Transwell and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL).

The miR-142-3p relative expression levels of A549 group, anemoside B4 group, inhibitor NC group and miR-142-3p inhibitor group were 1.00±0.14, 1.58±0.18, 1.60±0.21 and 1.12±0.16, respectively; the relative expression levels of HMGA1 protein were 1.00±0.23, 0.56±0.07, 0.59±0.08 and 0.95±0.21, respectively; the proliferation rates were (84.62±9.11)%, (62.15±7.20)%, (63.89±7.77)% and (76.35±8.11)%, respectively; the migration number was (156.23±17.54), (80.65±8.67), (82.15±8.96) and (111.55±12.75) cells, respectively; the apoptosis rates were (8.96±0.95)%, (32.56±3.56)%, (33.95±3.79)% and (16.89±1.92)%, respectively. The proliferation rates of si-NC group and si-HMGA1 group were (75.98±8.05)% and (64.52±7.25)%, respectively; the migration number was (118.85±12.98) and (86.95±9.21) cells, and the apoptosis rates were (17.58±2.02)% and (28.15±3.13)%, respectively. The above indexes in A549 group were compared with anemoside B4 group, miR-142-3p inhibitor group were compared with inhibitor NC group, si-HMGA1 group were compared with si-NC group, the differences were all with statistically significant (all P<0.05).

Anemoside B4 may inhibit proliferation and migration of NSCLC cells and promote apoptosis by regulating the miR-142-3p/HMGA1 axis.

To investigate the in vitro inhibitory effects of microRNA-28-5p (miR-28-5p) targeting G antigen 12I antibody (GAGE12I) on the proliferation, migration, and invasion of gastric cancer cells.

SGC-7901 cell were randomly divided into miR-28-5p group (miR-28-5p mimic), miR-NC group (miR-28-5p negative control mimic), shGAGE12I group (GAGE12I knockout) and blank group (GAGE12I not knockout). Cell proliferation, migration, and invasion capabilities were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay and invasion chambers. Bioinformatics analysis and luciferase activity assays were conducted to examine the interaction between miR-28-5p and GAGE12I.

The proliferation rates of miR-28-5p and miR-NC groups were (99.90±10.30)% and (48.25±4.15)%; the invasion rates were (145.57±14.52)% and (67.30±6.95)%; the mobility rates were (103.58±10.75)% and (43.18±4.26)%, respectively, the differences were statistically significant (all P<0.05). The proliferation rates of shGAGE12I group and blank group were (99.80±10.20)% and (35.50±3.58)%; the invasion rates were (142.70±13.65)% and (65.30±6.75)%; the mobility rates were (103.55±10.06)% and (48.38±4.52)%, respectively, the differences were statistically significant (all P<0.05). GAGE12I was the target of miR-28-5p.

MiR-28-5p negatively regulates GAGE12I and reduces the proliferation, invasion and migration of gastric cancer cells.

To explore the effects of aloe-emodin on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of pathological scar fibroblasts, as well as its regulatory mechanisms.

Proliferative scar fibroblasts (HSFb) were randomly divided into the following groups: HSFb control group (normal culture), HSFb low-dose group (25.00 μg·mL^-1 aloe-emodin), HSFb medium-dose group (50.00 μg·mL^-1 aloe-emodin), HSFb high-dose group (100.00 μg·mL^-1 aloe-emodin), and HSFb-PFT-α group (100.00 μg·mL^-1 aloe-emodin + 20.00 μmol·L^-1 p53-specific inhibitor PFT-α). Keloid fibroblast (KFb) cells were randomly divided into the following groups: KFb control group (normal culture), KFb low-dose group (25.00 μg·mL^-1 aloe-emodin), KFb medium-dose group (50.00 μg·mL^-1 aloe-emodin), KFb high-dose group (100.00 μg·mL^-1 aloe-emodin), and KFb-PFT-α group (100.00 μg·mL^-1 aloe-emodin + 20.00 μmol·L^-1 p53-specific inhibitor PFT-α). Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, Western blotting was performed to detect the expression of p53 and EMT-related proteins, apoptosis was measured using the TUNEL assay.

The cell survival rates of the KFb control group, KFb low-dose group, KFb medium-dose group, and KFb high-dose group were (100.00±5.17)%, (84.13±8.34)%, (73.81±7.62)% and (54.59±3.47)%, respectively; the cell survival rates of the HSFb control group, HSFb low-dose group, HSFb medium-dose group, and HSFb high-dose group were (100.00±6.77)%, (83.50±6.08)%, (71.43±2.70)% and (61.80±4.79)%, respectively. The relative expression levels of p53 protein in the KFb control group, KFb low-dose group, KFb high-dose group, and KFb-PFT-α group were 0.31±0.04, 0.52±0.04, 0.76±0.06 and 0.38±0.05, respectively; the relative expression levels of E-cadherin protein were 0.35±0.04, 0.58±0.08, 0.76±0.13 and 0.41±0.06, respectively; the apoptosis rates were (4.82±0.59)%, (11.72±1.68)%, (20.36±1.93)% and (12.46±1.28)%, respectively; the relative expression levels of p53 protein in the HSFb control group, HSFb low-dose group, HSFb high-dose group, and HSFb-PFT-α group were 0.37±0.03, 0.48±0.05, 0.65±0.07 and 0.46±0.04, respectively; the relative expression levels of E-cadherin protein were 0.26±0.03, 0.46±0.05, 0.63±0.08 and 0.34±0.05, respectively; the apoptosis rates were (4.89±0.28)%, (13.98±0.83)%, (21.51±1.08)% and (12.95±1.10)%, respectively. The differences between the KFb low- and high-dose groups and the KFb control group, the KFb-PFT-α group and the KFb high-dose group, the HSFb low- and high-dose groups and the HSFb control group, and the HSFb-PFT-α group and the HSFb high-dose group were statistically significant (P<0.05, P<0.01, P<0.001).

Aloe-emodin may inhibit the proliferation of pathological fibroblasts, EMT, and induce apoptosis by regulating the p53-related signaling pathway.

To investigate the mechanism of quercetin in promoting muscle regeneration in acute skeletal muscle injury.

Satellite cells were randomly divided into blank group (conventional culture), hydrogen peroxide (H₂O₂) group (100 μmol·L^-1 H₂O₂ treated cells for 24 h), quercetin group (10 μmol·L^-1 quercetin treated cells for 24 h), H₂O₂+quercetin group (100 μmol·L^-1 H₂O₂+10 μmol·L^-1 quercetin treated cells for 24 h). Cell proliferation was detected by cell counting kit-8 (CCK-8) method; protein expression was detected by Western blot assay; mitochondrial reactive oxygen species (ROS) levels and related indicators of mitochondrial respiration were detected by kit.

The 24 h proliferation rates of cells in blank group, quercetin group, H₂O₂ group and H₂O₂+quercetin group were (100.00±4.27)%, (148.79±13.17)%, (81.70±3.19)% and (120.83±8.81)%, respectively; the relative expression levels of superoxide dismutase 1 (SOD1) protein were 0.64±0.09, 0.76±0.09, 0.24±0.03 and 0.43±0.06, respectively; the relative expression levels of myosin heavy chain (MyHC) protein were 0.61±0.05, 0.67±0.06, 0.32±0.03 and 0.47±0.06, respectively; the fluorescence intensities of mitochondrial ROS were (52.56±1.97), (48.46±4.05), (119.53±13.06) and (102.91±8.93) a.u., respectively; the catalase (CAT) levels were (28.66±2.18), (35.62±3.89), (18.13±1.78) and (23.97±2.72) μmol·mg protein^-1, respectively; mitochondrial respiratory chain (MRC) complex Ⅰ levels were (19.77±1.01), (23.28±2.48), (9.87±1.01) and (14.19±0.75) μmol·mg protein^-1, respectively. The above indexes in quercetin group and H₂O₂ group were compared with blank group, the above indexes in H₂O₂+quercetin group were compared with H₂O₂ group, the difference was statistically significant (P<0.05, P<0.01, P<0.001).

Quercetin can promote mitochondrial respiration by clearing mitochondrial ROS levels, improve oxidative damage, and then promote satellite cell proliferation, which can promote muscle regeneration in acute skeletal muscle injury.

To investigate the effect of ganoderma lucidum polysaccharides (GLPS) on ferroptosis of hippocampal neuronal (HT22) cell lines induced by hydrogen peroxide (H₂O₂) and its mechanism.

The H₂O₂-induced HT22 cell injury model was first established in vitro. HT22 cells were divided into normal group (conventional culture), H₂O₂ group (200 μmol·L^-1 H₂O₂), GLPS group (200 μmol·L^-1 H₂O₂+100 μg·mL^-1 GLPS), H₂O₂+Fin56 group (200 μmol·L^-1 H₂O₂+5 μmol·L^-1 Fin56), H₂O₂+Fin56+GLPS group (200 μmol·L^-1 H₂O₂+5 μmol·L^-1 Fin56+100 μg·mL^-1 GLPS). The oxidative stress markers were detected by enzyme-linked immunosorbent assay (ELISA); the protein expression levels of iron death markers, nuclear factor erythroid2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot.

The contents of malondialdehyde (MDA) in normal group, H₂O₂ group, GLPS group, H₂O₂+Fin56 group and H₂O₂+Fin56+GLPS group were (5.56±0.61), (15.53±0.83), (6.51±0.29), (20.92±1.03) and (13.65±0.70) nmol·mL^-1; the contents of superoxide dismutase (SOD) were (37.93±1.37), (22.48±0.59), (37.81±2.56), (16.10±2.28) and (22.21±2.99) μg·mL^-1; Ferritin protein expression levels were 1.52±0.03, 1.22±0.07, 1.42±0.06, 0.64±0.02 and 0.93±0.13; GPX4 protein expression levels were 3.29±0.34, 1.91±0.18, 2.99±0.22, 1.13±0.07 and 2.45±0.05; Nrf2 protein expression levels were 0.90±0.01, 2.24±0.02, 2.97±0.07, 2.45±0.07 and 2.76±0.11; HO-1 protein expression levels were 1.58±0.02, 1.76±0.04, 2.29±0.06, 1.67±0.02 and 2.03±0.06, respectively. H₂O₂ group was compared with normal group and H₂O₂+Fin56 group, GLPS group was compared with H₂O₂ group, H₂O₂+Fin56+GLPS group was compared with H₂O₂+Fin56 group and GLPS group, the differences were statistically significant (P<0.05, P<0.01).

GLPS can improve lipid peroxide accumulation and iron metabolism disorder induced by H₂O₂ in HT22 cells by activating Nrf2/HO-1 pathway, thereby inhibiting the occurrence of ferroptosis.

To investigate the effects of sodium aescinate on the differentiation of human umbilical cord mesenchymal stem cells (HUMSC) into neural-like cells and its possible mechanism.

HUMSC cells were randomly divided into blank group, experiment-L group, experiment-M group and experiment-H group. All the cells were cultured with neurobasal medium (NM) medium, cells in experiment-L group, experiment-M group and experiment-H group were treated with 1.00, 2.00 and 4.00 mg·L^-1 sodium aescinate, respectively. The expression levels of neuron-like cells markers and synaptic markers were detected by reverse transcription-polymerase quantitative chain reaction (RT-qPCR) and Western blot.

The relative mRNA expression levels of microtubule-associated protein 2 (MAP-2) in blank group, experiment-L group, experiment-M group and experiment-H group were 1.00±0.14, 1.26±0.08, 1.74±0.16 and 2.30±0.20, respectively; the relative mRNA expression levels of growth associated protein 43(GAP43) were 1.00±0.10, 1.14±0.15, 1.34±0.15 and 1.53±0.11, respectively; the relative expression levels of synaptophysin(SYN) mRNA were 1.00±0.09, 1.15±0.08, 1.32±0.12 and 1.48±0.13, respectively; the expression levels of neurofilament heavy chain(NF-H) protein were 0.41±0.04, 0.50±0.06, 0.71±0.06 and 1.21±0.09, respectively; postsynaptic density protein 95(PSD95) protein expression levels were 0.27±0.04, 0.41±0.06, 0.52±0.04 and 0.68±0.06, respectively; silent information regulator 1(SIRT1) protein expression levels were 0.31±0.04, 0.52±0.06, 0.67±0.06 and 0.80±0.10, respectively. The above indexes in experiment-L group, experiment-M group and experiment-H group were compared with blank group, the differences were all statistical significant (P<0.05, P<0.01); the above indexes compared among experiment-L group, experiment-M group and experiment-H group, the differences were all statistically significant (P<0.05, P<0.01).

Sodium aescinate may induce the differentiation of HUMSC into neural-like cells by regulating SIRT1 in vitro.

To explore the omalizumab via microRNA (miR)-26a-5p reduced the inflammasome, or the NOD-like receptor themal domain associated protein 3 (NLRP3) mediated pyroptosis on airway remodeling in asthmatic rats, based on the inhibition of the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response protein 88 (MyD88)/nuclear factor kappa-B (NF-κB) signaling pathway.

Fifty SD rats were divided into control group, model group, omalizumab group, omalizumab+agomir NC group and omalizumab+miR-26a-5p agomir group, with 10 rats in each group. The control group was intraperitoneally injected with 0.9% NaCl; the model group established the asthma model; the omalizumab group was intraperitoneally injected with 100 mg·kg^-1·d^-1 omalizumab daily on the basis of model group; the omalizumab + agomir NC group received tail vein injection of agomir NC on the basis of the omalizumab group; the omalizumab+ miR-26a-5p agomir group received tail vein injection of miR-26a-5p agomir on the basis of omalizumab group. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissue; enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory factors; real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and fluorescence in situ hybridization (FISH) were used to detect the expression of miR-26a-5p; Western blotting (WB) was used to detect the pyroptosis and TLR4/MyD88/NF -κB pathway-related proteins expression levels.

The tube wall thickness in control group, model group and omalizumab group were (35.16±2.95), (52.94±4.63) and (44.07±3.78) μm; interleukin-13 (IL-13) levels were (18.23±3.94), (61.84±10.94) and (34.23±6.11) pg·mL^-1; interferon gamma (IFN-γ) levels were (68.43±11.59), (22.94±4.70) and (43.10±8.04) pg·mL^-1; miR-26a-5p mRNA were 1.00±0.15, 2.26±0.31 and 1.37±0.19. The relative expression levels of NLRP3 in control group, the model group, the omalizumab group, the omalizumab +agomir NC group and omalizumab+miR-26a-5p agomir group were 1.00±0.11, 3.21±0.47, 1.77±0.24, 1.69±0.27 and 2.53±0.38; the relative expression levels of TLR4 were 1.00±0.13, 2.54±0.39, 1.86±0.39, 1.90±0.30 and 2.24±0.34; the relative expression levels of MyD88 were 1.00±0.15, 1.97±0.26, 1.44±0.21, 1.41±0.18 and 1.69±0.23; the relative expression levels of NF-κB were 1.00±0.12, 2.88± 0.37, 1.83±0.29, 1.77±0.25 and 2.54±0.41, respectively. The differences of the above indexes were statistically significant when compared the model group with the control group, the omalizumab group with the model group, and the omalizumab+miR-26a-5p agomir group with the omalizumab+agomir NC group (P<0.05, P<0.01).

Omalizumab may reduce NLRP3 inflammasome-mediated pyroptosis by inhibiting the activation of TLR4/MyD88/NF-κB pathway, thus achieving omalizumab inhibited airway remodeling and improved lung function in bronchial asthmatic rats.

To explore the effect of fingolimod (FTY720) on depressive behavior in depressive disorder rats and its related mechanism.

The SD rats were divided into the following groups: Control group (normal feeding), model group (depression model construction), and low, medium, high groups (administering 0.1, 0.3 and 1.0 mg·kg^-1 FTY720 prior to constructing the depression model, respectively), with 10 rats in each group. The hippocampal tissue morphology was assessed using hematoxylin-eosin (HE) staining; depression symptoms were evaluated through the sucrose preference test; cognitive function was assessed using the Morris water maze test; neuronal apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL); levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway-related proteins were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence; dopamine (DA) content in different brain regions was analyzed by high-performance liquid chromatography.

After different treatments, the sugar-water preference rates in control, model and low, medium, high groups were (81.95±9.06)%, (59.72±8.32)%, (62.34±7.58)%, (68.08±7.94)% and (79.61±9.25)%, respectively; the escape latencies were (18.73±2.06), (34.25±3.87), (31.64±2.92), (25.97±2.43) and (19.86±1.95) s, respectively; apoptosis rates were (3.93±0.65)%, (28.75±5.94)%, (24.63±3.21)%, (15.27±2.58)% and (6.08±1.74)%, respectively; NLRP3 mRNA relative expression levels were 1.00±0.17, 4.89±0.64, 4.31±0.72, 2.52±0.58 and 1.87±0.25; ASC mRNA relative expression levels were 1.00±0.14, 2.67±0.53, 2.28±0.39, 1.54±0.26 and 1.39±0.21; DA contents in PFC region were (795.42±64.38), (547.93±52.65), (571.08±51.97), (662.45±73.89) and (748.96±81.53) μg·g^-1; DA contents in NAc region were (2 186.53±124.97), (1 672.84±109.25), (1 769.65±112.14), (1 904.27±106.63) and (2 065.92±127.58) μg·g^-1; DA contents in the VTA region were (1 765.83±108.29), (1 316.73±115.84), (1 378.52±94.36), (1 494.76±103.21) and (1 653.94±108.45) μg·g^-1. Compared with the control group, the above indexes in the model group were statistically significant (all P<0.001). Compared with the model group, the above indexes in the middle dose group were statistically significant (all P<0.05). Compared with the model group, the above indexes in the high dose group were statistically significant (all P<0.001).

FTY720 can regulate neuronal damage and cognitive function in depressed model rats, and its antidepressant mechanism may be related to inhibiting the activation of NLRP3 inflammasome pathway and increasing the content of DA in the neural circuit of PFC-ARC-VTA.