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Objective:To investigate the changes and clinical significance of plasma S100A1 protein, nuclear factor-κB p65 (NF-κB p65) and interleukin-6 (IL-6) levels in patients with acute ischemic cerebrovascular diseases.Methods:A total of 141 patients with acute ischemic cerebral infarction (AICI; AICI group) and 20 patients with transient ischemic attack (TIA; TIA group) who received treatment in Northern Jiangsu People's Hospital from April to November 2020 were included in this study. According to the volume of cerebral infarct, the AICI group was subdivided into small-volume cerebral infarct (SCI group, n = 78), moderate-volume cerebral infarct (MCI group, n = 32) and large-volume cerebral infract (LCI group, n = 31) groups. An additional 31 healthy controls who concurrently received physical examination were included as controls (HC group). S100A1, NF-κB p65, and IL-6 levels were compared between AICI, TIA and HC groups and between SCI, MCI and LCI groups. S100A1, NF-κB p65, and IL-6 levels were correlated with the National Institutes of Health Stroke Scale score and the volume of cerebral infarct. The receiver operating characteristic curve (ROC) was drawn to analyze the diagnostic value of S100A1, NF-κB p65, and IL-6 levels for AICI. Results:S100A1, NF-κB p65, and IL-6 levels in the AICI group were (230.96 ± 39.37) ng/L, (3.99 ± 0.65) mg/L, (13.32 ± 1.57) ng/L, respectively, which were significantly higher than (185.85 ± 43.24) ng/L, (3.58 ± 0.74) mg/L, (11.61 ± 1.67) ng/L in the TIA group ( t = 4.95, 2.39, 4.14, all P < 0.05) and (181.47 ± 27.39) ng/L, (3.51 ± 0.99) mg/L, (11.42 ± 2.34) ng/L in the HC group ( t = 6.54, 3.32, 5.55, all P < 0.05). There were no significant differences in S100A1, NF-κB p65, and IL-6 levels between TIA and HC groups (all P > 0.05). S100A1, NF-κB p65, and IL-6 levels in the LCI group were (254.25 ± 37.07) ng/L, (4.41 ± 0.45) mg/L, and (14.00 ± 1.40) ng/L, respectively, which were significantly higher than (225.42 ± 30.92) ng/L, (3.85 ± 0.64) mg/L, (12.77 ± 1.31) ng/L in the MCI group ( t = 3.04, 3.60, 3.20, all P < 0.05) and (223.98 ± 40.21) ng/L, (3.88 ± 0.66) mg/L, (13.27 ± 1.65) ng/L in the SCI group ( t = 3.79, 4.01, 2.25, all P < 0.05). There were no significant differences in S100A1, NF-κB p65, and IL-6 levels between MCI and SCI groups (all P > 0.05). S100A1 and NF-κB p65 levels in patients with AICI were positively correlated with the volume of cerebral infarct ( r = 0.24, 0.27, both P < 0.05). S100A1 and IL-6 levels in patients with AICI were positively correlated with the National Institutes of Health Stroke Scale score ( r = 0.24, 0.28, both P < 0.05). The areas under the curves plotting S100A1, NF-κB p65, and IL-6 levels against AICI diagnosis were 0.818, 0.667 and 0.754, respectively. The optimal cutoff values were 181.03, 3.50 and 10.79, respectively. The corresponding sensitivities were 95.0%, 76.6% and 97.2%, respectively, and the specificities were 37.3%, 45.1% and 49.0%, respectively. Conclusion:Increased S100A1, NF-κB p65, and IL-6 levels in patients with AICI are closely related to the severity of AICI.
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ObjectiveTo investigate the protective effect of tanshinoneⅡA on the expression of S100A1 protein after acute myocardial ischemia injury in rats.Methods Sixty Wistar rats were randomly divided into sham operation group, acute myocardial ischemia model group and tanshinoneⅡA pretreatment group by random number table. The acute myocardial ischemia model was established by thoracotomy and penetration of a thread and occlusion around the root part of the left anterior descending coronary artery, while the sham operation group was established only by thoracotomy and penetration of a thread around the root part of that artery but without occlusion; 3 days before the operation, in the tanshinoneⅡA pretreatment group, intraperitoneal injection of tanshinoneⅡA solution(at a dose of 1.5 mg/kg) was applied, while in the sham and acute myocardial ischemia groups, intraperitoneal injection of an equal volume of saline was given. Myocardial cell apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL), the levels of serum superoxide dismutase (SOD), malondialdehyde(MDA), creatine kinase(CK), lactate dehydrogenase(LDH) and S100A1 protein were examined and the level of expression of S100A1 protein in myocardial tissue was assayed by immunohistochemical staining and Western Blot.Results Compared with the sham operation group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 expression in myocardial ischemia group and tanshinoneⅡA pretreated group were significantly increased, while SOD activity was decreased obviously; compared with the myocardial ischemia model group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 protein expression were significantly reduced〔apoptosis rate:(32.1±4.2)% vs.(72.4±5.4)%, MDA(μmol/L): 9.1±2.2 vs. 17.3±5.2, CK(U/L): 83.3±12.2 vs. 107.5±12.4, LDH (μmol·s-1·L-1): 84.0±16.4 vs. 114.4±16.0, S100A1(μg/L): 37.6±6.0 vs. 78.4±8.6,P<0.05 orP<0.01〕, while the activity of SOD was increased markedly in tanshinoneⅡA pretreated group(kU/L:72.8±10.2 vs. 49.6±8.8,P<0.01). TUNEL staining showed that in the myocardial ischemia model group and tanshinoneⅡA pretreated group, the myocardial cells represented positive staining(brown-yellow in color), irregular in shape with nuclear pyknosis, cell detachment from the surrounding tissue and other characteristics. And in sham operation group,the staining of majority of cells was negative. The results of immunohistochemistry showed that S100A1 protein staining was relatively deep in the myocardial ischemia model group and tanshinoneⅡA pretreated group, and in the latter group, the color of S100A1 protein positive staining was not as deep as that in the former group. Western Blot showed that the S100A1 protein expression in myocardial ischemia model group was 2.8 folds of that of the sham operation group, while the S100A1 protein expression in tanshinoneⅡA pretreated group was significantly decreased compared with that of myocardial ischemia model group(bothP<0.05),which was 1.5 folds of that of the sham operation group.ConclusionTanshinoneⅡA may play a role in inhibiting the expression of S100A1 protein to protect against acute myocardial ischemia injury, suggesting that this agent have a potential effect for treatment of myocardial ischemia.
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Objective To investigate the effect of serum-deprivation on the changes of [ Ca2+ ] i and the protein release of S100A13 and fibroblast growth factor 1 ( FGF-1 ) in thyroid cancer TT cell,and to reveal the role of Ca2+in the protein release of S100Al3 and FGF-1.Methods The protein expressions of FGF-1 and S100A13 in TT cells under serum-deprivation were detected by Western blot.The released FGF-1 protein from TT cells in the supernatant fluid was detected by ELISA.Realtime dynamic examinations on the change of 1 h [ Ca2+ ] i in TT cells under serum-deprivation were detected by confocal laser scanning microscopy.Then,the effect of EGTA( 2.5 mmol/ L),BAPTA-AM (2.5 μmol/L)on distributions of the fluorescence of S100AI 3 and FGF-1 in TT cells under serumdeprivation for6 h were detected by indirect immunofluorescence.Results The expressions of FGF-1 and S100A13 in TT cells after serum-deprivation for4 h and 6 h were reduced( P＜0.05 or P＜0.01 ),but the released FGF-1 protein from TT cells in the supernatant fluid was elevated ( P＜0.05 or P＜0.01).Confocal laser scanning of Ca2+ imaging indicated that [ Ca2+ ] i of serum-deprivation TT cells maintained the relative stabilization within 23 win,but the rapid rise of [ Ca2+ ] i achieved peak value 1.6 μmol/L after 30 min,and remained stable for about 17 win,and thereafter 40 win slowly dropped to a low level From 40 win to 60 win the [ Ca2+ ] i was about 0.3-0.6 μ mol/L.The average [ Ca2+ ] i was higher than that in normal group,EGTA group,and BAPTA-AM group within 1 h.The protein expressions of S100A13 and FGF-1 did not drop obviously in EGTA group and BAPTA-AM group.Conlusion The release of S100A13 and FGF-1 from TT cell under serum-deprivation is possibly related with the change of [ Ca2+ ]i.Both Ca2+-chelating agents EGTA and BA PTA-AM are able to inhibit the rise of [ Ca2+ ] i and release of S100A 13 and FGF-1 from TT cells under serum-deprivation.
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S100A,a Ca2+-depending inotropic factor in the heart,is found decreased during hear failure. Increase of S100A1 protein expression can improve cardiac function by regulating Ca2+ transportation, inhibiting left ventricular remodeling, decreasing apoptosis,and restoring energy supply of failing heart. Therefore,recovery of S100A1 protein expression in the failing heart is an effective strategy for treatment of heart failure.