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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Merck KGaA 4-phenylbutyrate (4-pba) powder
Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress <t>inhibitor</t> <t>4-PBA</t> (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.
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Image Search Results


Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress inhibitor 4-PBA (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.

Journal: Ecotoxicology and environmental safety

Article Title: Biochemical mechanisms of tributyltin chloride-induced cell toxicity in Sertoli cells.

doi: 10.1016/j.ecoenv.2023.114725

Figure Lengend Snippet: Fig. 5. TBTCL-induced apoptosis and cell cycle arrest via ER stress and the inhibition of autophagy. (a) Levels of GRP78 and CHOP were detected in the presence of ER stress inhibitor 4-PBA (1 mM) in 15 P-1 cells. (b-c) TBTCL-induced apoptosis was rescued by the inhibition of ER stress. (d) Levels of autophagic markers P62 and LC3-II were detected in the presence of autophagy agonist Rapamycin (200 nM) rescue in TBTCL-treated 15 P-1 cells. (e-f) TBTCL-induced apoptosis was rescued by Rapamycin. Results are presented as mean ± SD. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compare with the respective control group.

Article Snippet: Autophagy agonists Rapamycin (HY-10219), Torin1 (HY-13003) and lysosomal inhibitor chloroquine (HY-17589A), ER stress inhibitor 4-PBA (HY-A0281) were purchased from Medchemexpress (Guangdong, China).

Techniques: Inhibition, Control