Collectively, these findings demonstrate that CD30L critically regulates asthma airway remodeling via the JNK/p38 MAPK pathway, strongly suggesting its therapeutic potential as a target for airway remodeling in asthma.

These findings identify inflammation-induced pyroptosis as a central driver of the pathological changes in PON-induced cardiotoxicity. Notably, our work highlights BMP-7's capacity to inhibit these disease-related alterations. Collectively, these results expand on the current knowledge of the mechanistic framework of PON-induced cardiotoxicity, while also emphasizing BMP-7 as a promising therapeutic candidate with potential translational relevance.

Pretreatment with the specific JNK inhibitor SP600125 reversed the increases cleaved PARP and caspase-3/-7 caused by gelsemine...The results of the present study collectively suggested that gelsemine induces apoptosis through a ROS- and JNK1/2 -co-regulated pathway. To the best of our knowledge, this study is the first to demonstrate that gelsemine may be a potential therapeutic agent for tongue SCC.

In addition, HM specifically inhibited uPAR expression levels, which were also decreased by the pharmacological mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor UO126 and Jun N-terminal kinase (JNK) inhibitor SP600125, in both CRC cell lines, including metastatic CRC (mCRC) SW620 cell line. Addition of HM to cells pretreated with JNK and MEK inhibitors attenuated the blockade of JNK and ERK phosphorylation and alleviated HM-downregulated uPAR expression and HM-inhibited mCRC cell migration. In conclusion, our in vitro studies demonstrate that HM exhibits an inhibitory effect on CRC migration and invasiveness, associated with uPAR downregulation through JNK and ERK pathways.

Specific inhibitors (SP600125, SB203580, NAC, Z-vad-fmk) were employed to validate the underlying mechanisms...Sch A selectively induces apoptosis in ESCC cells through ROS-JNK/p38-mediated pathways, mitochondrial dysfunction, and cell cycle arrest. These findings indicate that Sch A is a promising therapeutic candidate for treating ESCC.

This study demonstrates that YFBP exerts significant anti-OC therapeutic effects by modulating the inflammatory TME and activating the JNK/c-Jun pathway. Our findings provide a pharmacological basis for the traditional use of YFBP and highlight its potential as a promising candidate phytomedicine for OC therapy.

However, the JNK inhibitor (JNK-IN-8) suppressed the narciclasine-induced increase in cleaved caspase expression and apoptosis, whereas ERK and p38 inhibitors had no effect. These findings highlight the central role of JNK signaling in mediating extrinsic and intrinsic apoptotic pathways in osteosarcoma cells treated with narciclasine.

As the nuclear translocation of RB1CC1 was promoted by the JNK signaling pathway, SP600125, a JNK inhibitor, prevented the MPD-induced RB1CC1 nuclear translocation. In summary, MPD induced the dissociation of RB1CC1 from DRMs and its subsequent nuclear translocation, contributing to ferroptosis of prostate cancer cells.

The autophagy inhibitor chloroquine enhanced the pro-apoptotic effect of B. rynchopetera. Additionally, the c-Jun N-terminal kinase(JNK) inhibitor(SP600125) suppressed the activation of the JNK pathway as well as B. rynchopetera-induced apoptosis and autophagy. In conclusion, B. rynchopetera activates the MAPK/JNK pathway to induce apoptosis and autophagy, thereby exerting the therapeutic effect on LUAD.

WB was used to assess activation of the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) pathway, and pathway dependence was examined using the ROS scavenger N-Acetylcysteine (NAC) and the JNK inhibitor SP600125. It exerts anti-tumor effects by inducing oxidative stress and activating the JNK/p38 MAPK pathway in a ROS-dependent manner. These findings suggest that CSRNP1 may serve as a potential therapeutic target in the management of HCC.

These results suggest that BMP-7 might inhibit PON-induced cardiotoxicity. Furthermore, our findings pave the way for future translational studies with BMP-7, which can demonstrate the therapeutic potential of BMP-7 in a clinical setting.

Notably, claudin-11, an oligodendrocyte-specific, tight junction protein, was identified as a novel phospho-target that was highly reduced upon DJNKI-1 treatment. Together, these findings highlight potential molecular markers of anxiolytic response and suggest synaptic and metabolic interplay in mood regulation.