Fig 2: Lycorine hydrochloride induces apoptosis of BCL2-drug-resistant gastric cancer cell lines. a Screening of HA14–1 resistant cell lines (Detailed screening methods was described in the materials and methods). b Western blotting analysis of MCL1 expression in MKN-45-R and SGC-7901-R cell lines expressing shGFP, shMCL1#2, shMCL1#4. Trypan blue staining was used to analyze the apoptosis induced by DMSO or HA14–1 in MKN-45-R and SGC-7901-R cell lines expressing shGFP, shMCL1#1. c, d Apoptosis was analyzed in MKN-45-R, SGC-7901-R cells after treatment with 20 μM LH for 48 h by trypan blue and TUNEL staining. Apoptotic rate of MKN-45-R, SGC-7901-R cells in panel was quantified. e, f The expression of apoptotic protein, including C-Caspase 9, C-Caspase 3, PARP and C-PARP in BCL2-drug-resistant gastric cancer cells treated with LH at different concentrations and time gradients. DMSO was used as control. Tubulin was used as internal reference. All data were analyzed by unpaired Student’s t-tests and were showed as the means ± SD. *p < 0.05, **p < 0.01, ***p < 0.001

Fig 3: CFTR protein expression decreased in PA-induced endothelial cell injury. (a) PA induced a decrease in cell viability in HUVECs in a concentration-dependent manner. HUVECs were incubated with the indicated concentrations of PA for 24 h, and cell viability was determined by the MTT assay (n = 3). (b–d) Western blotting results of CFTR, caspase 3, and cleaved caspase 3 protein expression. HUVECs were incubated with PA (200 and 400 μM) or vehicle (BSA) for 24 h, and then, western blot was performed. ∗Versus BSA group, p < 0.05, n = 4.

Fig 4: Knockdown of miR-329-3p expression affects OGD-induced BV-2 cell activation and apoptosis. (A) BV-2 cells were transfected with inhibitor control or miR-329-3p inhibitor for 24 h, and then reverse transcription-quantitative PCR was performed to analyze the expression levels of miR-329-3p. (B) BV-2 cells were cultured in serum/glucose-free DMEM with 95% N2 and 5% CO2 at 37˚C for 48 h; then, the cells were transfected with inhibitor control or miR-329-3p inhibitor for 24 h and reverse transcription-quantitative PCR was performed to analyze the expression levels of miR-329-3p. (C) TNF-α release into the supernatant of the transfected cells was detected using ELISA. (D) NO production in the supernatant of the transfected cells was detected using a commercial kit. (E and F) Flow cytometric analysis was used to measure the levels of apoptosis of BV-2 cells induced by OGD. (G) Cleaved caspase-3 and caspase-3 protein expression was measured using western blotting. (H) Cleaved caspase-3/caspase-3 ratio. (I) Caspase-3 activity was detected using a colorimetric assay kit. **P<0.01 vs. inhibitor control; ##P<0.01 vs. control; &&P<0.01 vs. OGD + inhibitor control. SNHG1, small nucleolar RNA host gene 1; miR, microRNA; OGD, oxygen-glucose deprivation; NO, nitric oxide.

Fig 5: Lnc5745 inhibits DOX-induced cardiomyocyte apoptosis in NMVCs.a CCK-8 assays showing that lnc5745 overexpression increased NMVC viability under DOX treatment. b Lnc5745 inhibited caspase-3/7 activation stimulated by DOX in NMVCs. c Apoptotic cells were observed with the TUNEL method (green). The nuclei were stained with DAPI (blue). Scale bar, 200 μm. Lnc5745 overexpression decreased cell apoptosis induced by DOX. d Ratio of TUNEL-positive cardiomyocytes was determined by ImageJ (n = 200). e Lnc5745 knockdown reduced NMVC viability under DOX treatment. f Lnc5745 knockdown increased DOX-stimulated caspase-3/7 activity. g, h Apoptotic cells were observed with TUNEL method (green). Nucleus were stained by DAPI (blue). Lnc5745 knockdown further increased DOX-induced cardiomyocyte apoptosis. Scale bar, 200 μm. The results are from three independent experiments, *P < 0.05. Variables are presented as the mean ± SD.