BAX (BCL2-associated X protein)

In summary, we show HRK expression is distinctly regulated between different subtypes of naevi and melanoma, with supporting evidence this differential expression contributes to regulation of melanocytic proliferation.

These results suggest that E-BVL may influence apoptotic and proliferative pathways in THP-1 leukemia cells. Overall, this study highlights B. vulgaris leaf extract as a promising natural source of bioactive compounds for anti-leukemic research, without specifically implicating berberine, which was not detected in the extract.

Network pharmacology also revealed the involvement of SA1-4 and key targets-regulated SIRTs in neurodegeneration, including non-amyloidogenic cascade, tau phosphorylation, calcium homeostasis, insulin-mediated glucose uptake, and neuroinflammation. Therefore, SA1-4 exert promising multi-target therapeutic strategies against oxidative damage, potentially offering alternative anti-Alzheimer candidates for further clinical neurodegenerative and anti-aging therapeutics.

JC-1 staining showed the obvious MMP depolarization, and Western blot illustrated the increased expression of caspase-3 and Bax/Bcl-2 ratio during the cell apoptosis process. This study highlights the potential of GCP@NBs as novel and highly effective nanoplatforms for treatment of PDAC.

Atractylon treatment for 12 h activated autophagic flux, because atractylon-induced autophagy was abolished by 3-methyladenine but was enhanced by chloroquine or bafilomycin A1. Furthermore, loss of MMP and activation of caspases upon atractylon treatment were abrogated by 3-methyladenine or autophagy-related gene 3 (ATG3) siRNA in HepG2 cells, suggesting that autophagy activation was required for induction of apoptosis. Altogether, atractylon disrupted the PI3K/AKT/mTOR signaling leading to autophagy-dependent apoptosis, which could be a promising candidate for anti-hepatoma therapy.

HMB protects lungs in experimental sepsis by inhibiting NF-κB inflammation, reducing ER and mitochondrial apoptosis, and boosting antioxidant defenses via NRF2/GPX4. These findings support its potential as adjunct therapy for sepsis-induced ALI.

FZP may promote the apoptosis of tumor cells by activating the endogenous Bax/Bcl-2/cleaved Caspase-3 apoptosis pathway, which is mediated by mitochondria. These findings revealed the potential of FZP in the treatment of HCC and provided more treatment options for patients.

AST treatment mitigated these fibrotic changes, as evidenced by reductions in gene expression (p=0.001 for COL1A1 and p=0.005 for COL3A1) and improvements in Masson's trichrome staining. In conclusion, this study suggests that AST may confer a protective effect against BPA-induced testicular damage by reducing apoptosis and fibrosis; however, changes in oxidative stress markers did not achieve statistical significance. Furthermore, AST may enhance spermatogenesis.

Cytotoxicity was synergistic; however, apoptotic and stress indicators may be antagonistic. In clinical circumstances, caffeine may be an adjuvant in breast cancer treatment, however mechanistic and in vivo investigations are needed.

All compounds reduced ethanol-induced loss of viability and apoptosis, and PQM-242 additionally prevented ethanol-mediated Bax upregulation. Overall, PQM-242 and PQM-249 demonstrated enhanced cellular safety and maintained protective activity, supporting their further investigation as candidate molecules for AUD.

GA co-treatment significantly ameliorated these alterations, reducing inflammatory and apoptotic markers, restoring SIRT-1, and suppressing p53 activation. Collectively, GA exerts hepatoprotective effects through modulation of the TLR-4/NF-κB/IL-6 pathway and restoration of the SIRT-1/p53 regulatory axis, highlighting its immunopharmacological potential in sepsis-induced hepatic dysfunction.

Mechanistic studies revealed elevated intracellular reactive oxygen species (ROS) levels, activation of caspase-3, DNA damage, upregulation of pro-apoptotic genes (TP53 and bax), and downregulation of the anti-apoptotic gene bcl-2. These findings indicate that CI-ZnO-NPs induce caspase-mediated apoptosis in lung cancer cells through oxidative stress-dependent mechanisms, highlighting their promise as a biogenic nanotherapeutic approach for treating lung cancer.