Andrographolide stimulates p38 mitogen-activated protein kinase–nuclear factor erythroid-2-related factor 2–heme oxygenase 1 signaling in primary cerebral endothelial cells for definite protection against ischemic stroke in rats

Synthetic Ruthenium Complex TQ-6 Potently Recovers Cerebral Ischemic Stroke: Attenuation of Microglia and Platelet Activation

“…Subsequently, the cells were incubated with an anti-NF-κB p65 mAb for 2 h, washed with PBS, and then subjected to fluorescein isothiocyanate (FITC)-conjugated anti-rabbit IgG for 1 h. They were stained with 4',6-diamidino-2-phenylindole (DAPI; 30 µM) and mounted on a glass slide using a mounting buffer (Vector Laboratories). The fluorescence images were captured using a Leica TCS SP5 Confocal Spectral Microscope Imaging System (Mannheim, Germany) [21].…”

Andrographolide, A Natural Antioxidant: An Update

“…Andrographolide (10 µM) activates Nrf2 via its phosphorylation on ser 40 . A translocation of Nrf2 from the cytoplasm to the nucleus was also observed in cells treated with andrographolide (10 µM) after 30 min of treatment [85]. Primary culture of rat astrocytes treated for 1h with different concentrations of andrographolide showed an increase in Nrf2 protein.…”

“…Andrographolide increased HO-1 protein in the brain of Wistar rats treated with 0.1 mg/kg by intraperitoneal for 6 h [85]. It increased Nrf2 translocation and decreased Keap-1 mRNA expression in lung of BALB/c mice treated with 5 or 10 mg/kg andrographolide by intraperitoneal for 1 and 24 h [96].…”

“…Main effects of andrographolide on Nrf2 pathway in vivo, Symbols: " " for an increase, " " for a decrease, and "-" for not communicated. SOD activity (liver, kidney, heart, and red blood cells); CAT activity (heart); GSH peroxidase activity (kidney); GSH reductase (kidney, heart, and red blood cells); GSH S-transferase (liver); GSH protein (heart); antioxidant proteins (SOD1, GST Ya, GST Yb, HO-1, GCLC, and GCLM) (liver, kidney, and heart); mRNA (GCLC, GCLM, GST Ya/Yb, SOD1, and HO-1) (liver and kidney) [25] Wistar rats 0.1 mg/kg, intraperitoneal (6 h) -----HO-1 protein (brains) [85] BALB/c mice 5 or 10 mg/kg, intraperitoneal (1 and 24 h) --(lung) -mRNA (lung) HO-1, GR, GCLM, GPx-2, and NQO1 (mRNA) [96] BALB/c mice LPS/GalN (1 h) followed by andrographolide (2.5, 5, or 10 mg/kg), intraperitoneal (8 h) -(liver) ---HO-1 protein (liver) [6] C57BL/6 mice Acetaminophen (orally) every day for 6 weeks followed by andrographolide (20 or 40 mg/kg, orally) treatment every day at 2 weeks after acetaminophen administration --(liver) --ANDRO reversed the decreased hepatic expression of GCLC, GCLM and HO-1 mRNA expression induced by acetaminophen. Co-treatment with ANDRO (40 mg/kg) NQO1 mRNA [33] C57BL/6 mice Streptozotocin (intraperitoneal injection) for 5 consecutive days followed by andrographolide (1, 10, or 20 mg/kg/day) for 12 weeks by intragastric gavage (heart) ----SOD activity ; MDA and 4-HNE ; Nox2, Nox-4, p47 phox , Nrf2, and HO-1 mRNA [54] Balb/c mice Toluene diisocyanate treatment (dermally and intranasally) for asthma induction with andrographolide treatment (0.1, 0.5, or 1 mg/kg, prophylatic regimen) -(lung) ---HO-1 protein (1 mg/kg, lung) [97] Andrographolide increased Nrf2 protein in lung of Balb/c mice sensitized (dermally and intranasally) with toluene diisocyanate for asthma induction and treated with andrographolide 0.1, 0.5, or 1 mg/kg [97].…”

HO-1/EBP interaction alleviates cholesterol-induced hypoxia through the activation of the AKT and Nrf2/mTOR pathways and inhibition of carbohydrate metabolism in cardiomyocytes

“…Induction of HO-1 provides a protective function in the cardiovascular system through the effects of CO and bilirubin on various cells. HO-1 executes anti-apoptotic, anti-inflammatory, anti-hypertensive and anti-oxidant functions, and protects the cardiovascular system by the activation of the p55/TNFR-1, p38 MAPK and PI3K/AKT signaling pathways (4–6). Importantly, the HO-1 gene promoter sequence contains a large quantity of regulatory cis -elements, such as stress-responsive, hypoxia-responsive, and cadmium responsive elements and NF-κB binding sites (7–9).…”