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Research Paper

Carvedilol alleviates lipopolysaccharide (LPS)-induced acute lung injury by inhibiting Ras homolog family member A (RhoA)/ROCK activities

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Pages 4137-4145 | Received 12 Aug 2021, Accepted 22 Nov 2021, Published online: 21 Feb 2022

Figures & data

Figure 1. The effect of carvedilol on cell viability of LPS-induced BEAS2B cells. (a) The cell viability of BEAS2B cells treated with carvedilol. (b) The cell viability of LPS-induced BEAS2B cells treated with carvedilol. ***P < 0.001 Versus Control, ###P < 0.001 Versus LPS.

Figure 1. The effect of carvedilol on cell viability of LPS-induced BEAS2B cells. (a) The cell viability of BEAS2B cells treated with carvedilol. (b) The cell viability of LPS-induced BEAS2B cells treated with carvedilol. ***P < 0.001 Versus Control, ###P < 0.001 Versus LPS.

Figure 2. Carvedilol reduces the expression of RhoA and ROCK in LPS-induced BEAS2B cells. (a-b) The expression of RhoA in LPS-induced BEAS2B cells. (c) The expression of MYPT1 in LPS-induced BEAS2B cells. ***P < 0.001 Versus Control, ###P < 0.001 Versus LPS.

Figure 2. Carvedilol reduces the expression of RhoA and ROCK in LPS-induced BEAS2B cells. (a-b) The expression of RhoA in LPS-induced BEAS2B cells. (c) The expression of MYPT1 in LPS-induced BEAS2B cells. ***P < 0.001 Versus Control, ###P < 0.001 Versus LPS.

Figure 3. Carvedilol reduces the cell viability, inflammation and oxidative stress of LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. (a-b) The expression of RhoA after the plasmid overexpressing RhoA was constructed. ***P < 0.001 Versus Ov-NC. (c) The cell viability of LPS-induced BEAS2B cells transfected with Ov-RhoA. (d) The expression of inflammatory cytokines in LPS-induced BEAS2B cells transfected with Ov-RhoA, detected by ELISA. (e) The expression of inflammation-related markers in LPS-induced BEAS2B cells transfected with Ov-RhoA, detected by Western blot. (f) The levels of ROS, MDA, and SOD in LPS-induced BEAS2B cells transfected with Ov-RhoA *P < 0.05, ***P < 0.001 Versus LPS. ###P < 0.001 Versus LPS+5 µM+Ov-NC.

Figure 3. Carvedilol reduces the cell viability, inflammation and oxidative stress of LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. (a-b) The expression of RhoA after the plasmid overexpressing RhoA was constructed. ***P < 0.001 Versus Ov-NC. (c) The cell viability of LPS-induced BEAS2B cells transfected with Ov-RhoA. (d) The expression of inflammatory cytokines in LPS-induced BEAS2B cells transfected with Ov-RhoA, detected by ELISA. (e) The expression of inflammation-related markers in LPS-induced BEAS2B cells transfected with Ov-RhoA, detected by Western blot. (f) The levels of ROS, MDA, and SOD in LPS-induced BEAS2B cells transfected with Ov-RhoA *P < 0.05, ***P < 0.001 Versus LPS. ###P < 0.001 Versus LPS+5 µM+Ov-NC.

Figure 4. Carvedilol reduces apoptosis of LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. (a-b) The apoptosis of LPS-induced BEAS2B cells transfected with Ov-RhoA. ***P < 0.001 Versus LPS. ###P < 0.001 Versus LPS+5 µM+Ov-NC.

Figure 4. Carvedilol reduces apoptosis of LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. (a-b) The apoptosis of LPS-induced BEAS2B cells transfected with Ov-RhoA. ***P < 0.001 Versus LPS. ###P < 0.001 Versus LPS+5 µM+Ov-NC.

Figure5. Carvedilol affects the expression levels of apoptosis-related proteins in LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. The expression of apoptosis-related proteins, including Bax, Bad, cleaved caspase3 and Bcl-2 in LPS-induced BEAS2B cells transfected with Ov-RhoA. ***P < 0.001 Versus LPS. ##P < 0.01, ###P < 0.001 Versus LPS+5 µM+Ov-NC.

Figure5. Carvedilol affects the expression levels of apoptosis-related proteins in LPS-induced BEAS2B cells by inhibiting RhoA/ROCK activities. The expression of apoptosis-related proteins, including Bax, Bad, cleaved caspase3 and Bcl-2 in LPS-induced BEAS2B cells transfected with Ov-RhoA. ***P < 0.001 Versus LPS. ##P < 0.01, ###P < 0.001 Versus LPS+5 µM+Ov-NC.