AIM: To investigate the associations of aqueous humor miR-21 and miR-29b levels with the severity of optic nerve damage and GMPE in patients with primary open angle glaucoma(POAG).METHODS:POAG patients who presented to the hospital from May 2023 to May 2025 were prospectively enrolled as the disease group, and patients with cataract treated during the same period were included as the control group. Baseline characteristics and aqueous humor levels of miR-21 and miR-29b were compared between the two groups. POAG patients were categorized into mild and moderate-to-severe groups according to the mean deviation(MD)of visual field. Clinical characteristics and the expression levels of miR-21 and miR-29b in aqueous humor were compared between the two groups. Correlations and nonlinear associations between miR-21/miR-29b levels and RNFL thickness, visual field MD, and BMO-MRW were evaluated. Furthermore, factors influencing the progression of optic nerve damage were analyzed. Based on prognostic outcomes, patients were divided into good prognosis and poor prognosis groups, and the aqueous humor levels of miR-21 and miR-29b were compared. ROC curve analysis was performed to assess the predictive value of combined GMPE with miR-21 and miR-29b for prognosis in POAG patients.Internal validation and decision curve analysis(DCA)were also conducted.RESULTS:This study included 151 patients in the disease group(age 56.07±7.59 y, 84 males and 67 females)and 138 patients in the control group(age 56.84±8.25 y, 68 males and 70 females). There were 45 cases in the mild group(age 54.63±7.34 y, 27 males and 18 females)and 106 cases in the moderate-severe group(age 56.68±8.39 y, 57 males and 49 females). There were 118 cases in the good prognosis group(age 55.83±8.07 y, 67 males and 51 females)and 33 cases in the poor prognosis group(age 56.94±8.23 y, 17 males and 16 females). Compared with the control group, the disease group exhibited significantly higher miR-21 levels and lower miR-29b levels(all P<0.001). Compared with the mild group, intraocular pressure and miR-21 levels were significantly higher in the moderate-to-severe group, while RNFL thickness, visual field MD, BMO-MRW, and miR-29b levels were significantly lower(all P<0.01). The miR-21/miR-29b ratio was negatively correlated with RNFL thickness, visual field MD, and BMO-MRW(all P<0.05). Elevated intraocular pressure and miR-21 levels, reduced RNFL thickness, lower visual field MD, and decreased BMO-MRW and miR-29b levels were identified as risk factors for aggravated optic nerve damage in POAG patients(all P<0.05). Compared with the good prognosis group, the poor prognosis group showed significantly higher miR-21 levels and lower miR-29b, RNFL, and BMO-MRW levels(all P<0.001). The combined prediction model incorporating aqueous humor miR-21, miR-29b, RNFL, and BMO-MRW yielded significantly higher AUC and specificity for predicting POAG prognosis than individual parameters alone(both P<0.05). The ROC prediction model demonstrated good consistency, and the combined prediction model exhibited high clinical utility.CONCLUSION: Aqueous humor levels of miR-21 are significantly elevated while miR-29b levels are significantly decreased in POAG patients, and these alterations are closely correlated with the severity of optic nerve damage and GMPE parameters.

OBJECTIVETo evaluate whether atorvastatin inhibits oxidized low-density lipoproteins (Ox-LDL)-stimulated foam cell formation from THP-1 macrophages by regulating the activation of peroxisome proliferator-activated receptor γ (PPARγ) and nuclear factor-κB (NF-κB). Methods THP-1 macrophages were pretreated with 10, 20, or 40 µmol/L atorvastatin for 2 h, and after washing with PBS twice, the cells were incubated with 60 µg/ml of Ox-LDL for 48 h. The quantity of intracellular lipid of the cells was detected with Oil red O staining and enzymatic fluorometric method. The expression of the scavenger receptors of CD36 and SRA were analyzed with Western blotting. We also examined the effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and the activation of PPARγ and p-iκB, and further assessed the capacity of the macrophages to bind to Dil-oxLDL.

RESULTSAtorvastatin potently inhibited ox-LDL-induced macrophage-derived foam cell formation, down-regulated the expression of CD36 and SRA, and up-regulated the expression of ABCA1. Atorvastatin markedly suppressed the activation of PPARγ and p-iκB in ox-LDL-stimulated THP-1 macrophages (P<0.05) and significantly decreased the Dil-oxLDL-binding capacity of the macrophages (P<0.05).

CONCLUSIONAtorvastatin as an effective anti-atherosclerosis agent can suppress the activation of PPARγ and p-iκB to reduce lipid accumulation in macrophages.

ATP Binding Cassette Transporter 1 ; metabolism ; Atorvastatin Calcium ; Cell Line ; Foam Cells ; cytology ; drug effects ; Heptanoic Acids ; pharmacology ; Humans ; I-kappa B Proteins ; metabolism ; Lipoproteins, LDL ; metabolism ; Macrophages ; cytology ; drug effects ; NF-kappa B ; metabolism ; PPAR gamma ; metabolism ; Pyrroles ; pharmacology ; Signal Transduction ; drug effects ; Transcriptional Activation ; Up-Regulation

Objective To evaluate whether atorvastatin inhibits oxidized low-density lipoproteins (Ox-LDL)-stimulated foam cell formation from THP-1 macrophages by regulating the activation of peroxisome proliferator-activated receptorγ(PPARγ) and nuclear factor-κB (NF-κB). Methods THP-1 macrophages were pretreated with 10, 20, or 40μmol/L atorvastatin for 2 h, and after washing with PBS twice, the cells were incubated with 60 μg/ml of Ox-LDL for 48 h. The quantity of intracellular lipid of the cells was detected with Oil red O staining and enzymatic fluorometric method. The expression of the scavenger receptors of CD36 and SRA were analyzed with Western blotting. We also examined the effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and the activation of PPARγand p-iκB, and further assessed the capacity of the macrophages to bind to Dil-oxLDL. Results Atorvastatin potently inhibited ox-LDL-induced macrophage-derived foam cell formation, down-regulated the expression of CD36 and SRA, and up-regulated the expression of ABCA1. Atorvastatin markedly suppressed the activation of PPARγand p-iκB in ox-LDL-stimulated THP-1 macrophages (P<0.05) and significantly decreased the Dil-oxLDL-binding capacity of the macrophages (P<0.05). Conclusion Atorvastatin as an effective anti-atherosclerosis agent can suppress the activation of PPARγ and p-iκB to reduce lipid accumulation in macrophages.

Objective To evaluate whether atorvastatin inhibits oxidized low-density lipoproteins (Ox-LDL)-stimulated foam cell formation from THP-1 macrophages by regulating the activation of peroxisome proliferator-activated receptorγ(PPARγ) and nuclear factor-κB (NF-κB). Methods THP-1 macrophages were pretreated with 10, 20, or 40μmol/L atorvastatin for 2 h, and after washing with PBS twice, the cells were incubated with 60 μg/ml of Ox-LDL for 48 h. The quantity of intracellular lipid of the cells was detected with Oil red O staining and enzymatic fluorometric method. The expression of the scavenger receptors of CD36 and SRA were analyzed with Western blotting. We also examined the effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and the activation of PPARγand p-iκB, and further assessed the capacity of the macrophages to bind to Dil-oxLDL. Results Atorvastatin potently inhibited ox-LDL-induced macrophage-derived foam cell formation, down-regulated the expression of CD36 and SRA, and up-regulated the expression of ABCA1. Atorvastatin markedly suppressed the activation of PPARγand p-iκB in ox-LDL-stimulated THP-1 macrophages (P<0.05) and significantly decreased the Dil-oxLDL-binding capacity of the macrophages (P<0.05). Conclusion Atorvastatin as an effective anti-atherosclerosis agent can suppress the activation of PPARγ and p-iκB to reduce lipid accumulation in macrophages.