Journal: bioRxiv

Article Title: Palmitoleate Protects against Zika virus infection-induced Endoplasmic Reticulum Stress and Apoptosis in Neurons

doi: 10.1101/2025.01.22.634157

Figure Lengend Snippet: A. Immunoblot analysis showed an increase in p-IRE1α, increase in full length, and cleaved ATF6 at 8h – 32 h of post-infection time point when infected with 0.1 MOI rMR. B. An increase in p-eIF2α and s-XBP1 was detected at 72 h and 96 h of post-infections when the infected with 0.1 MOI rMR. Total (t)IRE1α and t-eIF2α levels were unaltered between mock and rMR-infected neuronal cells. C. Cells treated with Salubrinal (eIF2α dephosphorylation inhibitor, eIF2αi), and STF-083010 (IRE1αi, IRE1α endonuclease inhibitor) significantly decreased the apoptotic nuclei percentage and caspase 3/7 activity after 96 h of post-infection. Beta-actin was used as loading control and remained unchanged. The images are representative images. Data presented as mean ± SEM, n=3 or 4, *** p<0.001, **** p<0.0001 compared to mock or ZIKV infected cells.

Article Snippet: Pan caspase inhibitor Z-VAD-FMK (# S7023), IRE1α endonuclease inhibitor (# STF-083010), and Salubrinal (eIF2α dephosphorylation inhibitor) (# S2923) were acquired from Selleckchem, TX, USA.

Techniques: Western Blot, Infection, De-Phosphorylation Assay, Activity Assay, Control

Journal: bioRxiv

Article Title: Palmitoleate Protects against Zika virus infection-induced Endoplasmic Reticulum Stress and Apoptosis in Neurons

doi: 10.1101/2025.01.22.634157

Figure Lengend Snippet: SH-SY5Y cells were infected with 0.1 MOI rMR or PR and treated with PO (100 µM and 200 µM) at different post-infection time points (8 h, 72 h, 96 h). A. Immunoblot analysis showed that PO treatment of 200 µM decreased the p-IRE1α. B. cleaved ATF6 at 8 h of post-infection time point when infected with rMR. PO treatment (100 µM and 200 µM) decreased the C. p-IRE1α, D. p-eIF2α, and E. s-XBP1 at both 72 h and 96 h of post-infection time point when infected with rMR. F. PO treatment (100 µM and 200 µM) decreased the p-IRE1α and p-eIF2α when infected with PR at 96 h of post-infection time point.

Article Snippet: Pan caspase inhibitor Z-VAD-FMK (# S7023), IRE1α endonuclease inhibitor (# STF-083010), and Salubrinal (eIF2α dephosphorylation inhibitor) (# S2923) were acquired from Selleckchem, TX, USA.

Techniques: Infection, Western Blot

Journal: bioRxiv

Article Title: Palmitoleate Protects against Zika virus infection-induced Endoplasmic Reticulum Stress and Apoptosis in Neurons

doi: 10.1101/2025.01.22.634157

Figure Lengend Snippet: ZIKV infection induces caspase-dependent apoptosis and sustained ER stress activation in the neuronal cells. An increase in mitochondrial pro-apoptotic mediators BIM, and PUMA, and a decrease in anti-apoptotic mediators Bcl-2, Bcl-xL, and Mcl-1 are observed due to the ZIKV infection. Further, ZIKV infection results in the activation of caspases and increases the levels of cleaved PARP leading to neuronal apoptosis. Infection with ZIKV also causes sustained ER stress as evidenced by an increases the phosphorylation of IRE1α and eIF2α, cleavage of ATF6, splicing of XBP1, and CHOP. In contrast, when the ZIKV-infected neuronal cells are treated with palmitoleate it results in dramatic decrease in PUMA, caspase 3/7 activation, and cleaved PARP expressions. Similarly, the treatment of palmitoleate also reduces ER stress which is evidenced by a decrease in p-IRE1 α, p-eIF2 α, s-XBP1, cleaved ATF6, and CHOP. Further, treatment of palmitoleate also decreases the ZIKV replication in the neurons.

Article Snippet: Pan caspase inhibitor Z-VAD-FMK (# S7023), IRE1α endonuclease inhibitor (# STF-083010), and Salubrinal (eIF2α dephosphorylation inhibitor) (# S2923) were acquired from Selleckchem, TX, USA.

Techniques: Infection, Activation Assay

Journal: International immunopharmacology

Article Title: Inositol-requiring enzyme 1 alpha endoribonuclease specific inhibitor STF-083010 protects the liver from thioacetamide-induced oxidative stress, inflammation and injury by triggering hepatocyte autophagy.

doi: 10.1016/j.intimp.2019.04.051

Figure Lengend Snippet: Fig. 2. STF-083010 protects mice from TAA-induced liver injury. For survival experiments, the mice were subjected to a lethal dose of TAA administration (500 mg/ kg, n = 12/group). (A) Survival rate of TAA-treated mice with different concentrations of STF-083010 pretreatment at various time points. For injury experiments, the mice were subjected to a toxic dose of TAA administration (200 mg/kg, n = 6/group), and the liver tissues and serum samples were collected at 24 h after TAA treatment. (B, C) Serum ALT and AST levels. (D) Representative images of liver histopathology by H&E staining (magnification, ×100); the necrotic areas were exhibited. (E) Representative images of liver sections stained with TUNEL in green and DAPI in blue (magnification, ×100) and the quantification of TUNEL-positive cells. The data are represented as the means ± SEM. ⁎p < 0.05, compared with the CON group. #p < 0.05, compared with the TAA group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: To justify the effective dose of STF-083010 (MedChemexpress, New Jersey, MO, USA), separate groups of mice received intraperitoneal injection of different concentrations of STF-083010 (30, 50, 70mg/kg) dissolved in PBS 2 h prior to TAA administration.

Techniques: Histopathology, Staining, TUNEL Assay

Journal: International immunopharmacology

Article Title: Inositol-requiring enzyme 1 alpha endoribonuclease specific inhibitor STF-083010 protects the liver from thioacetamide-induced oxidative stress, inflammation and injury by triggering hepatocyte autophagy.

doi: 10.1016/j.intimp.2019.04.051

Figure Lengend Snippet: Fig. 3. STF-083010 alleviates TAA-induced oxidative stress and hepatic inflammation. (A) Representative images of liver sections stained with DHE (magnification ×100) and the relative fluorescence density. (B, C, D) The transcriptional levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in the liver tissues. The data are represented as the means ± SEM. ⁎p < 0.05, compared with the CON group. #p < 0.05, compared with the TAA group.

Article Snippet: To justify the effective dose of STF-083010 (MedChemexpress, New Jersey, MO, USA), separate groups of mice received intraperitoneal injection of different concentrations of STF-083010 (30, 50, 70mg/kg) dissolved in PBS 2 h prior to TAA administration.

Techniques: Staining

Journal: International immunopharmacology

Article Title: Inositol-requiring enzyme 1 alpha endoribonuclease specific inhibitor STF-083010 protects the liver from thioacetamide-induced oxidative stress, inflammation and injury by triggering hepatocyte autophagy.

doi: 10.1016/j.intimp.2019.04.051

Figure Lengend Snippet: Fig. 4. STF-083010 triggers autophagy in TAA-treated liver samples. The mice were subjected to a toxic dose of TAA administration (200 mg/kg, n = 6/group) in the presence or absence of STF-083010 and/or CQ pretreatment. The liver tissues and serum samples were collected at 24 h after TAA treatment. Western blot analysis for the expression levels of p-IRE1α, sXBP1, LC3B, p62, Beclin-1 and β-actin. The relative intensity is normalized to β-actin. The data are represented as the means ± SEM. ⁎p < 0.05, compared with the CON group; #p < 0.05, compared with the TAA group; $p < 0.05, compared with the TAA + STF group.

Article Snippet: To justify the effective dose of STF-083010 (MedChemexpress, New Jersey, MO, USA), separate groups of mice received intraperitoneal injection of different concentrations of STF-083010 (30, 50, 70mg/kg) dissolved in PBS 2 h prior to TAA administration.

Techniques: Western Blot, Expressing

Journal: International immunopharmacology

Article Title: Inositol-requiring enzyme 1 alpha endoribonuclease specific inhibitor STF-083010 protects the liver from thioacetamide-induced oxidative stress, inflammation and injury by triggering hepatocyte autophagy.

doi: 10.1016/j.intimp.2019.04.051

Figure Lengend Snippet: Fig. 5. STF-083010 alleviates TAA-induced oxidative stress, inflammation and liver injury by triggering autophagy in vivo. The mice were subjected to a toxic dose of TAA administration (200 mg/kg, n = 6/group) in the presence or absence of STF-083010 and/or CQ pretreatment. The liver tissues and serum samples were collected at 24 h after TAA treatment. (A, B) Serum ALT and AST levels. (C) Representative images of liver histopathology by H&E staining (magnification, ×100); necrotic areas were exhibited. (D) Representative images of liver sections stained with TUNEL in green and DAPI in blue (magnification, ×100) and the quanti- fication of TUNEL-positive cells. (E) Representative images of liver sections stained with DHE (magnification ×100) and the relative fluorescence density. (F, G, H) The transcriptional levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in the liver tissues. The data are represented as the means ± SEM. ⁎p < 0.05, compared with the CON group; #p < 0.05, compared with the TAA group; $p < 0.05, compared with the TAA + STF group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: To justify the effective dose of STF-083010 (MedChemexpress, New Jersey, MO, USA), separate groups of mice received intraperitoneal injection of different concentrations of STF-083010 (30, 50, 70mg/kg) dissolved in PBS 2 h prior to TAA administration.

Techniques: In Vivo, Histopathology, Staining, TUNEL Assay