Total cholesterol affects the outcome of patients with anterior cerebral artery-occluded acute ischemic stroke treated with thrombolysis.

OBJECTIVE: In this study, we investigated whether certain types of lipid profiles are major contributors of acute ischemic stroke (AIS). PATIENTS AND METHODS: We screened 13,285 hospitalized patients in two stroke medical centers treated with thrombolysis, thrombectomy, or conventional care for anterior cerebral artery-occluded AIS, and found 266 patients. We examined their plasma lipid profiles using the cutoff values from a receiver operating characteristic (ROC) curve. We applied a multivariate logistic regression or Fisher's exact test to compare their outcomes and risk factors. We used the modified Rankin scale (mRS) score to assess the major clinical outcome of the patients 3 months after disease onset. Mortality and symptomatic intracranial hemorrhage (sICH) were both evaluated as risk factors. We analyzed symptoms' improvements at discharge as a disease outcome measure. RESULTS: In the patients with anterior cerebral artery-occluded AIS (NIHSS ≥ 10) treated by intravenous (IV) thrombolysis, a total cholesterol (TC) level greater than 5.07 mmol/L predicted a poor outcome (OR 3.55, 95% CI 1.21,10.46, p=0.021). CONCLUSIONS: In patients with anterior cerebral artery-occluded AIS, the TC level is a promising prognosis marker for the IV thrombolysis outcome.

Phosphocreatine attenuates angiotensin II-induced cardiac fibrosis in rat cardiomyocytes through modulation of MAPK and NF-κB pathway.

OBJECTIVE: Transforming growth factor ß (TGF-ß) plays crucial roles in Ang II-induced cardiac fibrosis (CF). Phosphocreatine (PCr), one of the important players involved in cellular energy metabolism, is widely used in the treatment of clinical heart failure. However, whether it participates in CF is still unclear. This study aimed to identify the mechanisms involved in PCr and CF. MATERIALS AND METHODS: Rat cardiomyocytes (H9C2) were induced by Ang II followed by treatment of PCr. ERK1 siRNA, ERK2 siRNA and NF-κB siRNA were applied to identify the molecular mechanism. Then CF-related proteins were analyzed by western blot and real-time PCR to confirm the influence of the mechanisms involved in PCr. RESULTS: PCr did protect cardiomyocytes from Ang II-induced fibrosis. Meanwhile, PCr suppressed Ang II-induced up-regulation of TGF-ß. By detecting TGFß-mediated or MAPK pathway associated proteins, PCr inhibited MAPK and NF-κB pathway, thus suppressed Ang II-induced cardiac fibrosis, which was further confirmed by siRNA transfection. CONCLUSIONS: Our study determined that PCr protected cardiomyocytes from Ang II-induced CF through inhibition of MAPK and NF-κB pathway.