Journal: Nature

Article Title: Plasticity of the mammalian integrated stress response

doi: 10.1038/s41586-025-08794-6

Figure Lengend Snippet: ( a ) Representative western blot analysis of the indicated proteins in ΔuORF1 and WT mouse ES Cells treated with the inhibitor of PP1 phosphatase (containing GADD34 as a subunit), Salubrinal (15 μM, 5 h; ( n = 3 independent experiments). ( b,f ) Western blot analysis of the indicated proteins in MEFs expressing Con (shCon) or Eif2s2 (shEif2s2) shRNAs and treated with Tg (400 nM) (b) or Torin1 (250 nM) (f) for the specified times. Representative blots are shown ( n = 3 independent experiments). ( c-d ) Representative western blot analyses of the indicated proteins in MEFs treated with Tg (400 nM) for the specified durations, or MEFs expressing the indicated shRNAs, without (c) or with Tg-treatment (d) ( n = 3 independent experiments). Tg-treated MEFs in (c) were used as a positive control for induction of the c-ISR. ( e ) Representative western blot analysis of the indicated proteins in MEFs expressing control (shCon) or Eif2b5 shRNA (shEif2b5) and treated with (Tg-400 nM) or Torin1 (250 nM) of the specified durations ( n = 3 independent experiments). ( g-h ) Western blot analysis for the indicated proteins in MEFs expressing control (shCon) or Eif2b5 shRNA (shEif2b5) and treated with 4EGI-1 (200 μM) (g) Tg (400 nM) or SGC-CK2-1 (5 μM) (h) for the specified times. Representative western blots are shown ( n = 2 independent experiments). Lower eIF2α-p levels are consistent with GADD34 induction (h, 4 th lane). ( i ) Representative western blot analyses of the indicated proteins in MEFs treated with glucose (0 or 2.5 mM, 16 h). LiCl (10 or 25 mM) or Torin1 (250 nM) were used for the specified final hours of the 16 h treatment with medium containing 2.5 mM glucose ( n = 3 independent experiments).

Article Snippet: Chemicals used in this study: Tg (400 nM, Sigma-Aldrich T9033); sodium arsenite (1 mM, Sigma S7400); CPA (100 μM (BT474) and 200 μM (MEFs and mouse ES cells) Tocris number 1235); actinomycin D (10 μg ml −1 , Sigma-Aldrich A9415); cycloheximide (100 μg ml −1 , Sigma C7698); salubrinal (15 μM, Tocris number 3657); Torin 1 (250 nM, Tocris number 4247); LiCl (10 mM, Sigma); Herceptin (20 μg ml −1 , Genentech); 4EGI-1 (200 μM, Med Chem Express HY-19831); SGC-CK2-1 (5 μM, Cayman number 34103).

Techniques: Western Blot, Expressing, Positive Control, Control, shRNA

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 2. SAL inhibits LPS-stimulated apoptosis in kidney tissue and podocytes. (a) Representative images of TUNEL staining for each group. (b) The number of TUNEL-positive cells. (c) Flow cytometry was used for the assessment of cell apoptosis. (d) Quantification of apoptotic rate. Data are presented as mean ± SD (8 mice per group), and the cells experiment was performed in triplicates. Compared to the control group, ***p < 0.001; compared to LPS group, ##p < 0.01, ###p < 0.001.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques: TUNEL Assay, Staining, Flow Cytometry, Control

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 1. SAL alleviates LPS-induced acute kidney injury. (a) Serum creatinine and (b) BUN levels at 12 h after LPS intraperitoneal injection in each group of mice. (c) Effect of SAL on the serum level of NGAL; (d) Effect of SAL on the serum level of KIM-1. (e) Representative HE staining images of kidney tissues. Data are presented as mean ± SD (8 mice per group). Compared to the control group, ***p < 0.001; compared to LPS group, ###p < 0.001.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques: Injection, Staining, Control

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 3. SAL inhibits LPS-induced ROS production and oxidative stress. (a) Representative images of DHE staining in kidney tissue (red fluorescence). (b) Quantification of DHE fluorescence intensity. The extent of oxidative stress was evaluated by measuring (c) MDA content and (d) SOD activity in kidney tissue lysates (normalized to protein). Data are presented as mean ± SD (8 mice per group). Compared to the control group, ***p < 0.001; compared to LPS group, ###p < 0.001.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques: Staining, Activity Assay, Control

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 4. SAL promotes the autophagy of podocytes with LPS. (a) The cells were stained with LC3-II and DAPI. The cytoplasm of autophagy cells showed green fluorescence by LC3-II staining. (b) Each group’s proportion of autophagy cells was analyzed quantitatively (cells with LC3-II dots). (c) Representative gel blots depicting levels of autophagy-associated protein. Protein blots were quantified for (d) LC3-II and (e) p62. Cells experiment was performed in triplicates. Compared to the control group, ***p < 0.001; compared to LPS group, ###p < 0.001.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques: Staining, Control

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 5. SAL activates SIRT1 and Nrf2 pathways. (a) Representative gel blots of SIRT1 and Nrf2. These protein blots were quantified for (b) SIRT1 (normalized to GAPDH) and (c) nuclear Nrf2 (normalized to total PCNA). (d,e) The mRNA expression of Nrf2 downstream gene HO-1 and NQO1 (normalized to GAPDH). Data are presented as mean ± SD (8 mice per group). Compared to the control group, ***p < 0.001; compared to LPS group, ###p < 0.001.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques: Expressing, Control

Journal: Human & experimental toxicology

Article Title: Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

doi: 10.1177/09603271231169520

Figure Lengend Snippet: Figure 6. Model illustration on SAL-mediated protection on LPS- induced kidney injury, whose mechanisms are related to the regulation of SIRT1/Nrf2 pathways.

Article Snippet: For the LPS + SAL and SAL groups, the mice were pretreated with salidroside (SAL, 50 mg/kg, intraperitoneal injection, HYN0109, MedChemExpress) 2 h before LPS administration.

Techniques:

Journal: Burns & Trauma

Article Title: Nuclear fragile X mental retardation-interacting protein 1-mediated ribophagy protects T lymphocytes against apoptosis in sepsis

doi: 10.1093/burnst/tkac055

Figure Lengend Snippet: Ribophagy downregulated the PERK–ATF4–CHOP signaling pathway to alleviate ERS-related cell apoptosis in T lymphocytes. ( a – d ) Jurkat cells were pretreated with various concentrations of the upstream inhibitor salubrinal (Sal, 10, 20, 50 mM) for 2 h and then subjected to treatment with 500 ng/ml LPS for 24 h. Pretreatment with Sal, particularly at 20 mM, notably diminished LPS-induced ATF4 and CHOP expression and apoptosis. ( e-k ) Jurkat cells were pretreated with 20 mM Sal for 2 h and then treated with 500 ng/ml LPS for 24 h. Pretreatment with Sal markedly weakened LPS-induced ATF4 and CHOP expression and apoptosis. ( l , m ) Normal and NUFIP1-KD Jurkat cells were pretreated with 20 mM Sal for 2 h and then exposed to 500 ng/ml LPS for 24 h. Flow cytometric analysis showed that pretreatment with Sal obviously inhibited apoptosis compared with LPS alone. ( n – s ) The expression of PERK–ATF4–CHOP signaling pathway-related proteins in Splenic CD4 + T lymphocytes from WT and NUFIP1-deficient mice that were pretreated with 20 mM Sal for 2 h and then subjected to 500 ng/ml LPS for 24 h. ( t , u ) Flow cytometric analysis showed the apoptosis of Splenic CD4 + T lymphocytes in WT and NUFIP1-deficient mice with LPS stimulation or LPS plus Sal. One-way ANOVA was applied to test the statistical significance. Data are expressed as means ± SEM; * p < 0.05, * * p < 0.01, * * * p < 0.001. C control group, L lipopolysaccharide, S salubrinal, N normal, WT wild type, KD knockdown, CLP cecal ligation and puncture, NUFIP1 nuclear fragile X mental retardation-interacting protein 1, RES endoplasmic reticulum stress, PERK protein kinase RNA-like ER kinase, GRP78 glucose-regulated protein 78, ATF4 activating transcription factor 4, CHOP C/EBP homologous protein, 7-AAD 7-aminoactinomycin D, UL upper left, UR upper right, LL lower left, LR lower right, ANOVA analysis of variance, SEM standard error of mean

Article Snippet: Triton X-100 was purchased from Sigma, St. Louis, MO, USA and salubrinal (Sal) was obtained from Selleckchem, Houston, TX, USA.

Techniques: Expressing, Control, Knockdown, Ligation

Journal: Burns & Trauma

Article Title: Nuclear fragile X mental retardation-interacting protein 1-mediated ribophagy protects T lymphocytes against apoptosis in sepsis

doi: 10.1093/burnst/tkac055

Figure Lengend Snippet: Improvement in the 1-week survival rate of NUFIP1 gene-deficient mice subjected to CLP with salubrinal pretreatment. ( a ) The 1-week survival curves showed that the mortality rate of WT mice pretreated with 2 mg/kg Sal was lower than that of WT mice 1 week after CLP ( n = 10). ( b ) The 1-week survival curves of NUFIP1 gene-deficient mice ( n = 10); * p < 0.05, * * p < 0.01, * * * p < 0.001. WT wild type, KD knockdown, CLP cecal ligation and puncture, Sal Salubrinal, NUFIP1 nuclear fragile X mental retardation-interacting protein 1

Article Snippet: Triton X-100 was purchased from Sigma, St. Louis, MO, USA and salubrinal (Sal) was obtained from Selleckchem, Houston, TX, USA.

Techniques: Knockdown, Ligation