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1.
Figure 8

Figure 8. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

Trolox contributes to Nrf2-mediated protection of ATII cells from apoptosis, injury and inflammation induced by CS. CS generates oxidative stress, which is decreased by trolox and the activation of Nrf2. Lack of Nrf2 and this antioxidant compound leads to accumulation of ROS, induction of DNA damage, inflammation and p53-dependent apoptosis in ATII cells

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
2.
Figure 7

Figure 7. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

CS increases IL-8 and IL-6 levels in human primary ATII cells. Panel A—higher IL-8 (a) and IL-6 (b) levels in whole ATII cell extracts obtained from smoker in comparison with non-smoker lung donors as measured by ELISA. Panel B—smoking induces p53 mRNA expression in ATII cells isolated from smoker lung donors compared with non-smoker lung donors as measured by RT-PCR. * Statistically significant difference compared with non-smokers (P<0.05)

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
3.
Figure 4

Figure 4. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

Trolox decreases apoptosis in murine ATII cells exposed to CSE in vitro as detected by TUNEL assay. ATII cells were isolated from Nrf2+/+ (a) and Nrf2−/− (b) mice, treated with 0.5 trolox for 24 h and exposed to 4% CSE for 24 h. The percentage of apoptotic ATII cells is shown. * Statistically significant increase compared with control (P<0.05). #Statistically significant decrease compared with CSE alone. Representative pictures of TUNEL-positive (apoptotic) ATII cells are also shown

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
4.
Figure 5

Figure 5. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

High inflammatory response induced by CSE in murine ATII cells obtained from Nrf2−/− mice in vitro. KC (a) and IL-6 (b) levels in the ATII cell media were detected by ELISA. These cells were obtained from Nrf2−/− than Nrf2+/+ mice, cultured and treated with 4% CSE for 24 h. 0.5 μM trolox decreases inflammatory response induced by CSE. * Statistically significant increase compared with control (P<0.05). #Statistically significant decrease compared with CSE alone

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
5.
Figure 1

Figure 1. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

CS induces higher inflammation in Nrf2−/− mice than Nrf2+/+ mice, which was decreased by trolox. KC (a) and IL-6 (b) levels were measured by ELISA in BAL obtained from mice treated with trolox for 5 days and exposed to CS for 4 days in vivo as described in the Materials and Methods section. *—Statistically significant increase compared with control (P<0.05); &—statistically significant increase compared with Nrf2+/+ mice; and #—Statistically significant decrease compared with CS alone

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
6.
Figure 3

Figure 3. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

Trolox decreases murine ATII cell injury induced by CSE in vitro. ATII cells were isolated from Nrf2+/+ (a) and Nrf2−/− (b) mice and purified as described in the Materials and Methods section. ATII cells were treated with 0.5 μM trolox for 24 h followed by exposure to 4% CSE for 24 h. Lane 1—control; lane 2—PBS; lane 3—trolox; lane 4—CSE; and lane 5—trolox+CSE (immunoblotting). Relative expression of these proteins is also shown. * Statistically significant increase compared with control (P<0.05). #Statistically significant decrease compared with CSE alone

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
7.
Figure 2

Figure 2. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

Trolox abolishes CS-induced injury and apoptosis in ATII cells obtained from Nrf2+/+ mice in vivo. Mice were treated with trolox for 5 days and exposed to CS for 4 days in vivo as described in the Materials and Methods section. Panel A—protein expression in lung tissue; Panel B—protein expression in ATII cells. a—Nrf2+/+ mice; b—Nrf2−/− mice. Lane 1—control; lane 2—PBS; lane 3—trolox; lane 4—CS; lane 5—trolox+CS (immunoblotting). Relative expression of these proteins is also shown. Panel C—Paraffin-embedded lung sections were stained for proSP-C to identify ATII cells and with fluorescein to detect apoptotic cells by TUNEL assay. * Statistically significant difference compared with control (P<0.05). # Statistically significant decrease compared with CS alone

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.
8.
Figure 6

Figure 6. From: Trolox contributes to Nrf2-mediated protection of human and murine primary alveolar type II cells from injury by cigarette smoke.

Trolox decreases ROS generation, injury and inflammation in human primary ATII cells in vitro induced by CSE. Human ATII cells were treated with 10 μM trolox for 24 h followed by 6% CSE for 24 h. Panel A—ROS generation was decreased in ATII cells treated with trolox and CSE in comparison with CSE alone as measured by Amplex Red Hydrogen Peroxide Assay. Panel B—protein expression (immunoblotting): lane 1—control; lane 2—PBS; lane 3—trolox; lane 4—CSE; lane 5—trolox+CSE. Relative expression of these proteins is also shown. Panel C—CSE increases p53 and Nrf2 DNA-binding activity as determined by Transcription Factor Activation Array (P<0.05). RLU, relative light units. Panel D—IL-8 (a) and IL-6 (b) levels in ATII cell media as measured by ELISA. * Statistically significant increase compared with control (P<0.05). # Statistically significant decrease compared with CSE alone

E M Messier, et al. Cell Death Dis. 2013 April;4(4):e573.

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