Objective: The apoptotic effects of odoroside A on lung cancer cells were studied in our project. We also supported and extended our experimentally-proven results via bioinformatics analysis on human lung cancer tissues. Materials and Methods: In vitro studies were conducted using the A549 cell line. Cell proliferation was evaluated through a CCK-8 assay. For gene expression analysis, the qRT-PCR method was used, while CASP3 protein levels were detected using Western blotting and ELISA. Moreover, the oxidant status of cells was determined by measuring TAS and TOS levels. To construct a protein–protein interaction network, STRING analysis was performed. For the determination of differential expression of apoptosis-related genes, the GEPIA tool was utilized. Kaplan–Meier plots with overall survival, disease-specific survival and progression free intervals were obtained from UCSC Xena to evaluate the prognostic value of caspases. Results: The gene expression levels of CASP3, CASP7, CASP8, CASP9, FAS, and FADD were elevated between 4–16 fold in Odo A-treated lung cancer cells compared to controls. CASP3 protein expression was significantly higher in Odo A-treated cancerous cells than the control group. Low TAS (0.5700 ± 0.0067 in Odo A vs. 0.6437 ± 0.0151 in control) and high TOS (0.82800 ± 0.0208 in Odo A vs. 0.6263 ± 0.0258 in control) levels as well as high OSI values (1.4531 ± 0.0414 in Odo A vs. 0.9748 ± 0.0539 in control) were obtained. Correlogram and protein–protein network analyses suggested strong correlations and interactions among target genes. Lastly, Kaplan–Meier analysis showed no prognostic value of caspases, but potential therapeutic targets in lung cancer. Conclusions: Anti-cancer, prooxidative and therapeutic effects of Odo A on lung cancer cells were shown in our study. These data were supported and extended via computational analyses that we performed. In conclusion, Odo A could be used in clinics to treat patients with lung cancer.

Hepatocellular carcinoma is a progressive tumor with an aggressive nature. Despite many treatment options, survival rates remain low. In this study, the effect of Orox A on hepatocellular carcinoma cells was investigated. Hep3B cells were treated with a range of Orox A, and cell viability was assessed by MTT assays. Subsequent analyses using RT-qPCR demonstrated alterations in the expression of DNA damage and repair genes. To determine the damage in cancer cells, the amount of 8-OHdG and NO in the cells was measured by the ELISA method. Additionally, total antioxidant/oxidant status was measured, and the OSI value was calculated. Flow cytometry analysis was conducted to ascertain the specific cell cycle phase. The IC50 dose of Orox A for hepatocellular carcinoma cells was calculated to be 1385 μM at 24 h. According to the gene expression analysis results, NEIL1, OGG1, ATM and ATR gene expressions increased significantly, while APEX1 gene expression decreased significantly. The amount of 8-OHdG dramatically increased in cancer cells treated with Orox A, whereas the level of NO significantly decreased. Total antioxidant status (TAS) and total oxidant status (TOS) were significantly decreased in Orox A-applied cancer cells, and the oxidative stress index (OSI) was significantly increased. Flow cytometry analysis revealed that Orox A treatment caused G2/M phase arrest in the cell cycle. These findings collectively suggest that Orox A exerts cytotoxic effects on Hep3B cells through mechanisms involving DNA damage, oxidative stress, and cell cycle modulation, making it a promising candidate for further anticancer therapy development.

Background and Objectives: Alzheimer’s disease (AD) has become a serious health problem. Agomelatine (Ago) is a neuroprotective antidepressant. This study aimed to assess how Ago influences behavioral outcomes in AD-like rat model. Materials and Methods: Forty-eight Wistar albino rats were allocated into four groups: Control (C), Alzheimer’s disease-like model (AD), Alzheimer’s disease-like model treated with Ago (ADAgo), and Ago alone (Ago). Physiological saline was injected intrahippocampally in C and Ago animals, whereas Aβ peptide was delivered similarly in AD and ADAgo rats. On day 15, 0.9% NaCl was administered to the C and AD groups, and Agomelatine (1 mg/kg/day) was infused into ADAgo and Ago rats via osmotic pumps for 30 days. Behavioral functions were evaluated using Open Field (OF), Forced Swim (FST), and Morris Water Maze (MWM) tests. Brain tissues were examined histopathologically. Neuritin, Nestin, DCX, NeuN, BDNF, MASH1, MT1, and MT2 transcripts were quantified by real-time PCR. Statistical analyses were performed in R 4.3.1, with p < 0.05 deemed significant. Results: In the FST, swimming, climbing, immobility time, and mobility percentage differed significantly among groups (p < 0.05). In the MWM, AD rats exhibited impaired learning and memory that was ameliorated by Ago treatment (p < 0.05). DCX expression decreased in AD rats but was elevated by Ago (p < 0.05). Nestin levels differed significantly between control and AD animals; MT1 expression varied between control and AD cohorts; and MT2 transcript levels were significantly lower in AD, ADAgo, and Ago groups compared to C (all p < 0.05). Conclusions: Ago exhibits antidepressant-like activity in this experimental AD model and may enhance cognitive function via mechanisms beyond synaptic plasticity and neurogenesis.