Objective　To investigate the occurrence of postural hypotension (PH) in patients suffering from type 2 diabetes mellitus with or without hypertension (DMH or DM), and the relationship of PH and diabetic neuropathy, hyperinsulinemia and insulin resistance. Methods　A total of 30 cases of type 2 DM and 30 cases of DMH were included in this study. The blood pressure of all subjects were measured in supine and standing body positions respectively and PH was defined as a decline from supine to standing was ≥20 mmHg in systolic blood pressures (SBP). The concentrations of blood glucose and plasma insulin were measured to calculate the insulin sensitive index (ISI). Autonomic and peripheral function was determined by measuring the postural heart rates and the conduction speeds of superficial peroneal and communicating branch of peroneal nerves etc respectively. Results　Significant difference (P<0.01) was found in the occurrence of PH in the patients with DM (40%) and those with DMH (67%). The changes of postural blood pressure were more obvious in those with DM+PH and DMH+PH than in those with simple DM (P<0.01). The conduction speeds of newes were significantly lower in those with DMH+PH than with simple DM (P<0.05), but the occurrence of autonomic neuropathy had no difference between the 2 groups. There was no difference in postural heart rate, body mass index and blood glucose levels in fasting and 2 h after meal among the DM, DM+PH and DMH+PH groups. The concentrations of plasma insulin of those with DMH+PH were significantly higher, but their ISI significantly lower than those of the patients with DM respectively (P<0.01). The decline of postural SBP in patients with DMH+PH had a significantly positive correlation with their plasma insulin levels in fasting condition (r=0.689, P<0.01). Conclusion　The patients with DMH are more prone to PH compared with those only with DM and PH damages their peripheral nerves. Most of diabetic patients with PH suffer from obvious IR and hyperinsulinemia, and if with hypertension, the above metabolic disturbances are more severe.

Purpose: In this article, we aimed to investigate the influences of luteolin on inflammatory injury to cardiomyocytes induced by lipopolysaccharide (LPS). Materials and Methods: H9c2 cells were pretreated with different concentrations of luteolin (10, 20, and 50 μM) for 12 h and then stimulated with 10 μg/mL LPS or no LPS for 6 h. Cell viability was detected by CCK-8 assay. Cell apoptosis was determined by flow cytometry. QRT-PCR and Western blotting were utilized to examine mRNA and protein levels. ELISA was used to determine the levels of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin (IL)-6, IL-1β, and IL-18 in cell supernatants among different groups of H9c2 cells. Immunofluorescence was applied to evaluate reactive oxygen species formation in H9c2 cells. M-mode images of echocardiography, the ejection fraction test, fractional shortening test, end-systolic volume test, and end-diastolic volume test of mouse heart function were obtained by ultrasonic electrocardiogram. Results: Luteolin could alleviate inflammatory damage and inflammatory factor expression among LPS-induced H9c2 cells. Additionally, we found that luteolin decreased LPS-stimulated inflammatory damage in H9c2 cells by down-regulating NOD-like receptor family pyrin domain containing 3 (Nlrp3). Luteolin also improved myocardial function in mice treated with LPS and reduced myocardial relaxation. Luteolin reversed myocardial histological abnormalities in mice and reduced inflammation and cardiomyocyte apoptosis. Additionally, luteolin inhibited oxidative stress-mediated myocardial and systemic tissue damage in mice. Finally, luteolin reduced LPS-induced inflammatory damage in mouse cardiomyocytes by down-regulating Nlrp3. Conclusion We found that luteolin could reduce inflammatory damage to cardiomyocytes induced by LPS by down-regulating Nlrp3.