PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34480999-13 2022 The results demonstrated that HC067047 treatment decreased the protein levels of proapoptotic proteins such as Bax and caspase-3 in the hippocampus of SCP mice. Scopolamine 151-154 caspase 3 Mus musculus 119-128 34371027-4 2021 In the molecular level these changes are monitored as reduced oxidative load followed by significantly lower lipid peroxidation and protein carbonylation, increased superoxide dismutase, catalase, acetylcholinesterase, caspase-3 activity and glutathione content followed by higher expression of anti apoptotic protein bcl-2 in mice brain as compared to scopolamine (1 mg/kg bw) treated mice. Scopolamine 353-364 caspase 3 Mus musculus 219-228 30478761-6 2019 We also found that scopolamine promoted neuronal loss by inducing Bax, Pro-Caspase-3, and Caspase-3 and reducing the levels of the antiapoptotic protein Bcl-2. Scopolamine 19-30 caspase 3 Mus musculus 75-84 27346436-7 2016 Our results revealed that 1 h scopolamine pre-treatment induced cytotoxicity by increasing apoptotic cell death via oxidative stress-mediated caspase 3 activation and mitochondrial dysfunction. Scopolamine 30-41 caspase 3 Mus musculus 142-151 24386444-9 2013 The increase in ROS level and caspase-3 activity in the brain of scopolamine-treated mice were antagonized by the ME treatment. Scopolamine 65-76 caspase 3 Mus musculus 30-39 31141948-9 2019 EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining. Scopolamine 51-62 caspase 3 Mus musculus 162-171