Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis.

BACKGROUND: We studied the protective effects of Qingyi decoction (QYD) (a Traditional Chinese Medicine) against severe acute pancreatitis (SAP)-induced myocardial infarction (MI). AIM: To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP. METHODS: Ultrasonic cardiography, hematoxylin and eosin staining, immunohistochemistry, qRT-PCR, western blot, enzyme-linked immunosorbent assays, and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats. RESULTS: Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms, mortality rate, and ultrasonic cardiography outputs among the different groups compared to the control. The expression of serum cytokines [interleukin (IL)-1ß, IL-6, IL-8, IL-12, amyloid ß, and tumor necrosis factor-α] were significantly higher in the SAP versus QYD treated group (P < 0.05 for all). STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage (P < 0.001). There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups. The SAP group had a significantly higher apoptosis index score compared to the QYD group (P < 0.001). CONCLUSION: QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression (STIM1 and Orai1).

Increased expression of STIM1/Orai1 in platelets of stroke patients predictive of poor outcomes.

BACKGROUND AND PURPOSE: The platelet activation that is mediated by store-operated Ca2+ entry via stromal interaction molecule (STIM1) and Orai1 Ca2+ influx channels has been shown to play a key role in ischaemic stroke (IS). This study aimed to evaluate the impact of platelet STIM1/Orai1 protein expression on outcomes of IS. METHODS: A total of 160 patients with acute non-cardioembolic IS, among whom 45 patients had small-vessel diseases and 115 patients had large-vessel diseases, were evaluated. Patients were divided into two groups according to their baseline platelet STIM1/Orai1 protein expression: high-expression group (HG) (n = 80) and low-expression group (LG) (n = 80). Univariate and multivariate regression models were used to assess the correlation between STIM1/Orai1 expression and clinical outcomes, which included stroke severity that was measured based on the National Institutes of Health Stroke Scale and Stroke Impact Scale (SIS) at baseline and during the 3-month follow-up. RESULTS: There were no significant differences in age, sex and cardiovascular risk factors between patients in HG and LG. However, HG had very high levels of biomarkers such as glycosylated hemoglobin, C-reactive protein, homocysteine and high mobility group box-1 protein (all P < 0.05). Although the baseline stroke severity (National Institutes of Health Stroke Scale score) was not obviously higher in HG than in LG, patients showed a better recovery score (SIS score) in LG than in HG (90.75 ± 13.65 vs. 80.68 ± 7.09; P = 0.022). STIM1/Orai1 expression was an independent predictor of the 3-month stroke recovery (hazard ratio, 4.543; 95% confidence interval, 1.941-29.145; P = 0.029). CONCLUSIONS: A high expression level of platelet Orai1/STIMI1 was associated with poor clinical outcome (mortality and recurrence) and functional recovery (SIS scores) during the 3-month follow-up. Thus, we propose that these proteins are strongly predictive of life quality in patients with IS.