Display Settings:

Items per page
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 7

1.
Fig. 2

Fig. 2. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Myocardial cannabinoid CB1 and CB2 receptors, gp91phox, and TNF-α gene expression. Values are means ± SE of 6–15 experiments in each group. *P < 0.05 vs. young mice; #P < 0.05 vs. aging FAAH+/+ mice.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
2.
Fig. 4

Fig. 4. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Myocardial markers of apoptosis (PARP cleavage, caspase-3/7 activity, and caspase-3 and -9 gene expression). Values are means ± SE of 5–15 experiments in each group. *P < 0.05 vs. young mice; #P < 0.05 vs. aging FAAH+/+ mice.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
3.
Fig. 7

Fig. 7. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Effect of AEA on TNF-α-induced NF-κB activation in HCAECs. Representative immunofluorescence images of NF-κB activation in endothelial cells. TNF-α markedly activated NF-κB (note the intense nuclear staining). AEA significantly inhibits TNF-α-induced activation of NF-κB. Images shown are representative of 3 independent experiments yielding identical results.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
4.
Fig. 6

Fig. 6. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Effect of AEA on TNF-α-induced monocyte adhesion to HCAECs. HCAECs were treated as described in legend to Fig. 5. Top: representative images depicting monocytes adhered to the endothelial cells. Bottom: quantification of monocyte adhesion to endothelial cells. Values are means ± SE; n = 6. *P < 0.05 vs. control; #P < 0.05 vs. TNF-α. Paragraph symbol: P < 0.05 vs. AEA + TNF-α.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
5.
Fig. 3

Fig. 3. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Myocardial inducible nitric oxide synthase (iNOS) protein expression, nitrotyrosine formation, and matrix metalloproteinase (MMP)-2 and -9 gene expression. Values are means ± SE of 5–15 experiments in each group. *P < 0.05 vs. young mice; #P < 0.05 vs. aging FAAH+/+ mice.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
6.
Fig. 1

Fig. 1. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Hemodynamics in young (2- to 3-mo-old) and aging (28-to 31-mo-old) mice measured by the Millar pressure-volume conductance catheter system. Values are means ± SE of 7–11 experiments in each group. LVEDP, left ventricular end-diastolic pressure; LVSP, left ventricular systolic pressure; −dP/dt, diastolic decrement; tau (τ), relaxation time constant; FAAH, fatty acid amide hydrolase. *P < 0.05 vs. young mice; #P < 0.05 vs. aging FAAH+/+ mice.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.
7.
Fig. 5

Fig. 5. From: Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase.

Effect of anandamide (AEA) on TNF-α-induced ICAM-1 and VCAM-1 expression in human coronary artery endothelial cells (HCAECs). Values are means ± SE; n = 6. Cells were treated with either TNF-α (50 ng/ml) or AEA (15 μM) for 6 h or pretreated with AEA with the indicated concentrations followed by treatment with TNF-α for 6 h, and then cell surface ELISA was performed as described in MATERIALS AND METHODS (A and B). VC, vehicle control. A: ICAM-1 expression. *P < 0.05 vs. controls; #P < 0.05 vs. TNF-α. B: VCAM-1 expression. *P < 0.05 vs. controls; #P < 0.05 vs. TNF-α. Cells were pretreated with CB1/CB2 antagonists (1 μM) from 1 h before and during the treatment with TNF-α ± AEA (15 μM) as indicated for 6 h, and cell surface ELISA was performed (C and D). C: ICAM-1 expression. *P < 0.05 vs. control; #P < 0.05 vs. TNF-α. Paragraph symbol: Pg< 0.05 vs. AEA + TNF-α. D: VCAM-1 expression. *P < 0.05 vs. control; #P < 0.05 vs. TNF-α. Paragraph symbol: P < 0.05 vs. AEA + TNF-α.

Sándor Bátkai, et al. Am J Physiol Heart Circ Physiol. ;293(2):H909-H918.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk