p p38mapk  (Bioss)

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Effects of OST on cardiac autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques: Transmission Assay, Electron Microscopy, Western Blot

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Effects of OST on autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice after SB203580 administration. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-mTOR and mTOR. (H) Quantitative analysis of p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). # P < 0.05, ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group; ▲ P < 0.05, ▲▲ P < 0.01 vs the TRZ + OST H group.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques: Transmission Assay, Electron Microscopy, Western Blot

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Schematic illustration summarizing the protective effects of OST against TRZ-induced cardiotoxicity by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques:

Journal: Nature Metabolism

Article Title: Inhibition of IRAK4 by microbial trimethylamine blunts metabolic inflammation and ameliorates glycemic control

doi: 10.1038/s42255-025-01413-8

Figure Lengend Snippet: ( a ) Confirmation of a physical interaction between TMA and IRAK4 using TMA at concentrations ranging from 0.1 nM to 100 µM, resulting in a dissociation constant ( K d ) of 14 nM. ( b – e ) Physical interaction test between TMA and the four hits identified using a kinome screen, using TMA concentrations ranging from 0.1 nM to 100 µM for ( b ) ANKK1, ( c ) HIPK2, ( d ) JAK2 and ( e ) NDR1. For (b-e) N = 2 biological repeats. IRAK4 kinase activity is not significantly inhibited by choline ( f ), TMAO ( g ) or DMB ( h ), while TMA does not have any inhibitory effect on IRAK-1 kinase activity (average of N = 2 biological repeats) ( i ). ( j , k ) Phosphorylation for pThr183/Tyr185 SAPK/JNK/SAPK/JNK ( j ) and pThr180/Tyr182 p38MAPK/p38MAPK ( k ) densitometric ratios, represented by each dot. Data are means ± s.e.m. One-way ANOVA followed by Tukey’s post hoc tests (superscript letters for factor levels P < 0.05) on log-transformed data. Source data are provided.

Article Snippet: Membranes were immunoblotted with antibodies against the following proteins: p Thr345/Ser346 IRAK4 (11927), IRAK4 (4363), p Ser176/180 IKKαβ (2694), IKKβ (8943), p Thr183/Tyr185 SAPK/JNK (4668), SAPK/JNK (9258), p Thr180/Tyr182 p38MAPK (9215) and p38MAPK (9212), all purchased from Cell Signaling Technology, and β-actin (sc-47778, Santa Cruz Biotechnology).

Techniques: Activity Assay, Phospho-proteomics, Transformation Assay