Illustrations
Figure 1
Dex increased cell viability and inhibited cell apoptosis under OGD/R condition. (A) MTT assay was used to examine the viability of WRL-68 cells treated with OGD/R or Dex. (B) Representative pictures of WRL-68 cell apoptosis measured by flow cytometry. (C) Apoptosis cells were quantified. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 1
Figure 2
Dex attenuated inflammation and oxidative response in OGD/R-treated WRL-68 cells. ELISA assay was used to detect the release level of IL-6 (A), IL-1β(B), TNF-α (C), ROS (D), MDA (E), SOD(F), and GSH-Px (G) in WRL-68 cells treated with OGD/R or Dex. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 2
Figure 3
Dex activated Nrf2/HO-1 pathway and inhibited caspase pathway in OGD/R-treated WRL-68 cells. The relative mRNA expression levels of Nrf2 (A) and HO-1 (B) were measured by qRT-PCR in WRL-68 cells treated with OGD/R or Dex. (C) The protein level of Nrf2 and HO-1 was detected via western blot assay. (D) Quantitative analysis of protein band gray in figure 3 C . (E) The protein levels of Bax, Bcl-2, caspase3, and caspase9 were measured by western blot assay in WRL-68 cells treated with OGD/R or Dex. (F) Quantitative analysis of protein band gray in figure 3 E . GAPDH was used as internal control. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 3
Figure 4
Nrf2 knockdown partially abolished OGD/R-induced cell viability suppression and apoptosis. (A) The relative mRNA expression of Nrf2 was evaluated by qRT-PCR in WRL-68 cells treated with sh-Nrf2. (B) MTT assay was used to examine the viability of WRL-68 cells treated with OGD/R, Dex or sh-Nrf2. (C) Representative pictures of WRL-68 cell apoptosis measured by flow cytometry. (D) Apoptosis cells were quantified. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 4
Figure 5
Nrf2 knockdown reversed the effects of Dex on inflammation and oxidative response in OGD/R-treated WRL-68 cells. ELISA assay was used to detect the release level of IL-6 (A), IL-1β (B), TNF-α (C), ROS (D), MDA (E), SOD (F), and GSH-Px (G) in WRL-68 cells treated with OGD/R, Dex, or sh-Nrf2. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 5
Figure 6
Nrf2 knockdown attenuated the effects of Dex on apoptosis-related proteins in OGD/R-treated WRL-68 cells. The relative mRNA expression levels of Nrf2 (A) and HO-1 (B) were measured by qRT-PCR in WRL-68 cells treated with OGD/R, Dex, or sh-Nrf2. (C) The protein level of Nrf2 and HO-1 was detected via western blot assay in WRL-68 cells treated with OGD/R, Dex, or sh-Nrf2. (D) Quantitative analysis of protein band gray in figure 6 C . (E) The protein levels of Bax, Bcl-2, caspase3, and caspase9 were measured by western blot assay in WRL-68 cells treated with OGD/R, Dex, or sh-Nrf2. (F) Quantitative analysis of protein band gray in figure 6 E . GAPDH was used as internal control. All the results were shown as mean ± SD (n = 3), which were three separate experiments performed in triplicate. * p < 0.05 and ** p < 0.01.
Figure 6
Auteurs
Department of Anesthesia (Clinical Research Center for Anesthesiology of ERAS in Hunan Province), Hunan provincial people's hospital (First Affiliated Hospital of Hunan Normal University), Changsha 410005, P.R.China
* Correspondence: Dr. Bing-Bing Pan, Department of Anesthesia (Clinical Research Center for Anesthesiology of ERAS in Hunan Province), Hunan provincial people's hospital (First Affiliated Hospital of Hunan Normal University), No.61, West Jiefang Road, Furong District, Changsha 410005, Hunan Province, P.R.China: B-B. Pan
Background Dexmedetomidine (Dex), frequently used as an effective sedative, was reported to play a critical role in the protection of multiple organs. However, its underlying mechanism of a putative protective effect on ischemia/reperfusion (I/R)-induced liver injury is still unclear.