OBJECTIVETo investigate the temporal changes of serum interleukin-37 (IL-37) concentration following acute ST-segment elevation myocardial infarction (ASTEMI) and the relationship between IL-37 and C-reactive protein (CRP) in patients with ASTEMI.

METHODSThis analysis was conducted in a cohort of 20 patients with an established diagnosis of ASTEMI and 26 patients admitted for chest pain but with normal findings in coronary angiography (control) between June 2012 and December 2013. Venous blood was collected at days 1, 3, 5, and 7 after myocardial infarction for measurement of serum IL-37 and CRP levels using enzyme-linked immunosorbent assay (ELISA).

RESULTSCompared with the control group, the patients in ASTEMI group showed a significant acute elevation of IL-37 level on day 1 following myocardial infarction; IL-37 level reached the peak on day 3 and began to decrease on day 5, followed by a significant decrease on day 7. The time course of post-infarction CRP changes was consistent with that of IL-37 variations and showed a positive correlation the latter (r=0.63, P<0.05).

CONCLUSIONIL-37 may participate in the inflammatory responses in ASTEMI.

C-Reactive Protein ; metabolism ; Coronary Angiography ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-1 ; blood ; Myocardial Infarction ; blood

Objective:To analyze the effect of Croton leaf on ERK1/2 pathway in hippocampal of rats with cerebral ischemia-reperfusion.Methods:A total of 216 SD male rats were divided into sham operation group, model group, nimodipine group, low-dose, medium-dose and high-dose groups of croton leaf according to random nubmer table method, with 36 rats in each group. The MACO model of rats was prepared by the method of wire embolization. The high, medium and low dose groups were intragastrated with the water decoction 0.06 g/ml, 0.12 g/ml and 0.18 g/ml of Croton leaf; nimodipine group was intragastrated with nimodipine suspension 1.08 g/L; sham operation group and model group were intragastrated with equal volume of normal saline. Garcia JH score was used to conduct neurological function score, and HE staining was used to observe the morphology of hippocampal neurons after 7 days of continuous administration. Apoptosis of hippocampal CA3/DG region was detected by TUNEL assay. Western Blot was used to detect the expression of ERK1/2 and p-ERK1/2 proteins.Results:Compared with the model group at simultaneous point, the neurological function scores of low-dose, medium-dose and high-dose groups of Croton leaf increased ( P<0.01), the number of apoptotic cells decreased ( P<0.01), the expression of p-ERK1/2 / ERK1/2 [1 d: (0.22±0.03, 0.34±0.02, 0.46±0.01 vs. 0.19±0.02); 3 d: (0.38±0.02, 0.50±0.02, 0.68±0.02 vs. 0.27±0.02); 7 d: (0.29±0.03, 0.43±0.02, 0.59±0.02 vs. 0.21±0.03)] in hippocampus of the low-dose, medium-dose and high-dose groups of Croton leaf significantly increased ( P<0.01). Conclusion:Croton leaf could regulate the expression of ERK1/2 pathway protein upward, effectively improve the neural function and resist the apoptosis of hippocampal CA3/DG area of rats with cerebral ischemia-reperfusion injury.

BACKGROUND:Croton cream can activate ERK pathways and have anti-apoptotic effects on neuronal cells.It is not clear whether it synergistically exerts anti-apoptotic effects by inhibiting the activation of JNK and p38 pathways. OBJECTIVE:To explore the effects and mechanisms of croton cream on neuronal damage and apoptosis in the ischemic cortex of rats with cerebral ischemia-reperfusion injury. METHODS:(1)Ninety Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream low-dose group,croton cream medium-dose group,croton cream high-dose group and nimodipine group,with 15 rats in each group.Except for the sham operation group,animal models of middle cerebral artery occlusion were prepared in rats by the thread method.Rats in the three croton cream groups were given 20,40,and 60 mg/kg croton cream,respectively.Rats in the sham operation and model groups were given the same amount of normal saline,once a day,for 7 consecutive days.The optimal concentration of croton cream,namely the high dose of croton cream,was selected based on neurological deficit score,TTC staining,brain tissue water content,hematoxylin-eosin staining and Nissl staining.(2)Another 120 Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream group,JNK inhibitor group,croton cream+JNK inhibitor group,p38 MAPK inhibitor group,croton cream+p38 MAPK inhibitor group,and nimodipine group,with 15 rats in each group.Animal models of middle cerebral artery occlusion were prepared using the thread method in all the groups except in the sham operation group.Thirty minutes before modeling,10 μL of SP600125(JNK inhibitor)and 10 μL of SB203580(p38 MAPK inhibitor)were injected into the lateral ventricle of the rats,respectively.Rats in croton cream groups were intragastrically given 60 mg/kg croton cream.Seven days later,the JNK/p38 MAPK signaling pathway,apoptosis-related proteins and cell apoptosis were detected by western blot,TUNEL staining and flow cytometry,respectively. RESULTS AND CONCLUSION:(1)Compared with the sham operation group,neurological deficit score,cerebral water content,cerebral infarction volume and apoptosis rate were significantly increased in the model group(P<0.05),where nerve cells showed scattered distribution.Compared with the model group,neurological deficit score,water content of brain tissue and cerebral infarction volume were significantly decreased in the croton cream medium-dose group,high-dose group and nimodipine group(P<0.05),and the pathological morphology of nerve cells was significantly improved.(2)Compared with the JNK inhibitor group,p-JNK/JNK,p-p38/p38 and Bax expressions in rat brain tissue and the apoptotic rate were significantly decreased in the croton cream+inhibitor groups(P<0.05),while the expression of and Bcl-2 was significantly increased(P<0.05).To conclude,croton cream may inhibit the activation of JNK/p38 MAPK signaling pathway and reduce neuronal apoptosis to achieve neuroprotective effects in rats with cerebral ischemia-reperfusion injury.