Protective effects of lavender oil on sepsis-induced acute lung injury via regulation of the NF-κB pathway.

CONTEXT: Lavender oil (Lav) from Lavandula angustifolia L. (Lamiacease) exhibits antioxidative and anti-inflammatory properties against various diseases. OBJECTIVE: The study explores the effect of Lav pre-treatment on sepsis-induced acute lung injury (ALI). MATERIALS AND METHODS: Sprague-Dawley rats were assigned into Sham, caecal ligation and puncture (CLP), CLP + Lav (200, 400, and 800 mg/kg) groups. Lav was administered by gavage, once a day, for 7 days. Histological analysis was performed using haematoxylin and eosin staining. Cytokine and nitrite levels were detected by enzyme-linked immunosorbent assay kits and Griess reagent. Gene and protein expression were tested by quantitative real-time polymerase chain reaction and western blot. RESULTS: The levels of tumour necrosis factor-α (BALF: 64%, serum: 59%), interleukin (IL)-1ß (BALF: 63%, serum: 66%) and IL-6 (BALF: 54%, serum: 59%), and nitrite (40%) and inducible nitric oxide synthase (51%), and the level of myeloperoxidase (66%) and malondialdehyde (59%), and cleaved-caspase 3 (84%) and Bax expression (74%) induced by CLP were decreased when given Lav. Additionally, the level of superoxide dismutase (211%) and glutathione (139%), and the expression of Bcl-2 (980%) induced by CLP were increased when given Lav. The increased p-nuclear factor (NF)-κB/NF-κB (72%) and p-inhibitor of κBα (IκBα)/IκBα (77%) induced by CLP could be reversed by Lav. DISCUSSION AND CONCLUSIONS: Lav pre-treatment might protect rats from sepsis-induced ALI via deactivation of the NF-κB pathway. Our research demonstrated the regulatory mechanisms of Lav in sepsis-induced ALI and can provide a theoretical basis for the use of Lav in the treatment of sepsis-induced ALI.

L-arginine attenuates high glucose-accelerated senescence in human umbilical vein endothelial cells.

OBJECTIVE: Endothelial dysfunction is a key event in the onset and progression of atherosclerosis associated with diabetes. Increasing cell senescence may lead to endothelial dysfunction and contribute to vascular complications. Therefore, we aimed to elucidate the possible role and mechanism of L-arginine in preventing cell senescence induced by high glucose. METHODS: HUVECs were respectively cultured under normal control glucose (5.5mM), high glucose (33mM), co-incubation with L-arginine (800microM)and high glucose, and senescence was identified by beta-galactosidase staining, change of cell cycle and telomerase activity. Akt and eNOS activity was analyzed by western blot. RESULTS: High glucose significantly increased number of beta-galactosidase-positive stained cells, inhibited telomerase activity, increased proportion of cells in the G(0)/G(1) phase and reduced proportion in the S phase, and decreased NO synthesis. L-arginine significantly attenuated these senescent alterations. Furthermore, high glucose induced a decrease in Akt and eNOS activity, and L-arginine prevented the decrease in activity. The PI3K inhibitor LY294002 or eNOS inhibitor L-NAME attenuated anti-senescence effect of L-arginine. CONCLUSION: L-arginine may have an anti-senescence effect via the PI3K/Akt pathway in HUVECs exposed to high glucose and it might be a therapeutic agent for diabetic vascular complications.