This study aimed to determine the protective role of 1,8-cineol in Aroclor-1254 induced liver toxicity in a rat model. 1,8-cineol may be a protective agent due to its anti-apoptotic effect, reduction of oxidative damage, anti-inflammatory efficacy, and amelioration of histopathological changes in liver toxicity.

DB attenuates OGD/R-tempted oxidative stress, apoptosis, and mitochondrial dysfunction in HT22 hippocampal neurons by activating PINK1/Parkin-mediated mitophagy.

Curcumin regulates several signaling pathways linked to neuroprotection, such as those that reduce oxidative stress, prevent Aβ formation, and decrease neuroinflammation.

VDR and AHR are important mediators that determine the fate of immune cells.

Combination of FICZ and Vitamin D3 enhances Th17 and Th2 cell populations.

AHR antagonist modifies the prevalence of Th1 cells and associated ratios.

The ligand binding domain (LBD) of AHR is well accommodated with vitamin D.

d-Mannose upregulates TES via the NF-κB pathway to inhibit breast cancer proliferation.

Downregulation of circ_26782 in spinal neurons results in the upregulation of miR-19b-2-5p, which subsequently suppresses the expression of Rab1b. This suppression leads to the inhibition of the autophagy pathway, as evidenced by the downregulation of LC3-II/LC3-I expression, and consequently promotes axon growth.

In this study, 1,2,4-triazine compounds (Tr-1, Tr-2, Tr-3) on AChE and GST enzymes were explored. Also, their effects on liver cancer cell line (HepG2) were investigated. Finally, the study was theoretically docking and the results were evaluated.

The main purpose of this study was to investigate the antioxidant and anticarcinogenic effects of TQ, which has many traditional uses and is naturally found in Nigella sativa seeds, on the neoplastic changes induced by azaserine in exocrine pancreatic acinar cells. For this purpose, the anticarcinogenic effects of TQ given in the early period when AACFs were not yet formed (first month) and in the late period after AACFs were formed (third month) were investigated.

Development of Gall Bladder cancer by different methylation patterns and targeted therapies by inhibiting the molecular modulators.

Natural compounds and pharmacological interventions targeting molecular stress responses, oxidative stress, and protein aggregation may offer therapeutic strategies for Alzheimer's Disease (AD), aiming to alleviate neuroinflammation and promote neuroprotection.

We aim to search the promising hub genes of anxiety disorder using public gene datasets from Gene Expression Omnibus database. The expression of hub genes in anxiety disorders was further determined by constructing an anxiety mice model. Furthermore, as a candidate gene of interest, we explored the potential molecular regulatory mechanism of STAG2 in anxiety disorders using an in vitro model. PTPRC, SMC3, STAG2, FLT3, SYNE1, TERF2IP, NIPBL, ZFP451, MLLT3, and JAK1 were identified as anxiety-related hub genes. STAG2 was chosen as the primary target of our research, which was downregulated in the anxiety mice. Furthermore, STAG2 overexpression increased proliferation while inhibiting apoptosis in CORT-induced PC12 cells. Notably, overexpression of STAG2 caused a decrease in the expression of cGAS and STING in CORT-induced PC12 cells.

Activation of GPER1 by raloxifene and fulvestrant enhanced locomotor activity and mitigated oxidative stress, apoptosis, inflammation, and GFAP expression in haloperidol-induced tardive dyskinesia (TD) in rats. The neuroprotective effects of raloxifene and fulvestrant are attributed to GPER1-mediated activation of the PI3K/Akt/Nrf2/HO-1 signaling pathways.

The current work elucidates the expression pattern and role of circ_PSD3 in PTC, confirming that inhibition of circ_PSD3 is capable of inhibiting the proliferation and migration of PTC cells. More importantly, this is the first elucidation that circ_PSD3 promotes PTC progression and EMT via the regulation of the miR-145-5p/miR-338-3p/HMGB3 axis.

This study presents the synthesis and biological evaluation of novel quinazolin-4(3H)-one-thiazolidine-2,4-dione hybrids as dual inhibitors of α-Gly and ALR2. In vitro assays identified compound 9 as the most potent inhibitor (α-Gly K_i = 0.355 µM, ALR2 K_i  = 0.106 µM), with computational studies supporting its activity. Low cytotoxicity and favorable ADME-T profiles highlight the therapeutic potential of these compounds.

This study investigated Tirzepatide's effects on U87 glioma cells, showing it inhibits proliferation and migration while inducing ferroptosis through increased lipid peroxidation, elevated ROS and MDA levels, reduced SOD activity, and altered expression of iron (Ferritin, TFR1) and lipid metabolism genes (ACSL4, GPX4). Tirzepatide downregulated the SOX2/SLC7A11 axis, crucial for ferroptosis resistance, with effects reversed by Fer-1 or SOX2 overexpression. These findings highlight Tirzepatide's potential as a therapeutic strategy for glioma by targeting ferroptosis.

Isoliquiritigenin alleviates Ochratoxin A-induced hepatic oxidative stress and toxicity in Swiss albino mice via activating the PI3K/AKT/Nrf2 signaling pathway, hence augmenting antioxidant defense and cellular protection.