Jatrorrhizine Hydrochloride alleviates tert-butyl hydroperoxide-induced endothelial cell injury through its anti-inflammatory activity and PPAR-γ activation.

The aim of this study was to investigate whether Jatrorrhizine hydrochloride (JAH) can attenuate oxidative damage of endothelial cells by regulating mitochondrial function and inflammatory response. It was found that JAH inhibited tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in mouse brain endothelial cells (MBECs) by increasing cell viability and inhibiting cell apoptosis. Moreover, JAH significantly inhibited the production of reactive oxygen species (ROS) and lipid peroxidation. It enhanced mitochondrial membrane potential (MMP) and maintained ATP synthesis. In addition, JAH regulated the expressions of inflammatory cytokines and increased the activation of endothelial nitric oxide synthase (eNOS). The protective effect of JAH was related to the protein expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) gene. In conclusion, these results suggest that JAH may have therapeutic potential for ischemic stroke associated with endothelial dysfunction through its antioxidant and anti-inflammatory properties.

High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects.

OBJECTIVE: Evidence shows that salt can modulate adiponectin and inflammation levels in normal individuals. Therefore, we hypothesized that abnormalities in adiponectin and inflammation might be the potential mechanism of salt sensitivity. The aim of this study was to investigate whether different alterations of adiponectin and inflammation levels in response to a high-salt intake were exhibited between normotensive salt-sensitive and salt-resistant subjects. METHODS: Thirty normotensive subjects (25 to 50 y old) were selected from a rural community of northern China. They were sequentially maintained on a normal diet for 3 d at baseline, a low-salt diet for 7 d (NaCl 3 g/d), and then a high-salt diet for 7 d (18 g/d). RESULTS: Salt sensitivity was diagnosed in 10 subjects who exhibited an increase of at least 10% in mean blood pressure from the low-salt to the high-salt periods. Plasma adiponectin was significantly higher with the high-salt intake than with the low-salt intake (6.1 ± 1.3 versus 7.1 ± 1.7 µg/mL, P = 0.047) in normotensive salt-resistant subjects but not in the normotensive salt-sensitive subjects (6.4 ± 2 versus 5.9 ± 2.1 µg/mL, P = 0.481). The high-salt intake markedly increased plasma tumor necrosis factor-α (P < 0.0001) and monocyte chemoattractant protein-1 (P < 0.0001) in normotensive salt-sensitive and salt-resistant subjects. No significant change in plasma high-sensitivity C-reactive protein was observed. CONCLUSIONS: Our data indicate that the disturbance of adiponectin exists in normotensive salt-sensitive subjects during a high-salt diet, which may be a novel underlying mechanism of salt sensitivity.