Background & objectives: Several studies have provided evidence that opioids may play a role in cancer recurrence and metastasis. Multiple research data indicate that morphine can act as a proliferative or suppressive agent on tumour cells depending on the applied concentration. Therefore, this study was aimed to investigate whether the presence of clinically relevant concentrations of morphine has any effect on the efficacy of paclitaxel, a widely used chemotherapeutic drug, on the viability and apoptosis of human triple-negative breast cancer cell line. Methods: MDA.MB.231 cells were treated with paclitaxel in the presence or absence of morphine and examined for cell proliferation by the MTT assay. In addition, the effect of morphine on paclitaxel-induced apoptosis was investigated by flow cytometric assay and by the ratio of Bax/Bcl-2 mRNA expression levels with quantitative real-time (qRT)-PCR. Results: Morphine significantly increased the proliferation of breast cancer cells at low concentrations (0.1-2.5 µM) but higher concentrations showed cytotoxic effect. Pre-treatment with 0.1 or 1 µM of morphine decreased the paclitaxel-induced cytotoxicity, the proportion of apoptotic cell, and the ratio of Bax/Bcl-2 mRNA expressions. Interpretation & conclusions: Our data suggest that morphine promotes breast cancer cell viability at clinically relevant plasma concentrations and reduces the apoptotic effect of paclitaxel. This interaction may be very important in clinical settings; however, more studies are needed to explore the plausible mechanisms of interaction and to correlate such findings through in vivo animal studies as well as clinically.

The search for alternative, cost‐effective, and side‐effect‐free therapies for hyperlipidemia remains a priority. This study evaluated the effects of probiotic Lacticaseibacillus casei ATCC 393, prebiotic d ‐tagatose, and their synbiotic combination on hyperlipidemia induced in BALB/c mice via a high‐fat, high‐cholesterol diet over 12 weeks. During the final 4 weeks, different groups received the respective treatments. Compared to the positive control (PC) group, synbiotic administration (SYN group) significantly reduced serum glucose by 32.8%, total cholesterol by 20.2%, HDL‐C by 28.0%, and triglycerides by 42.5% ( p < 0.05). Although serum albumin, alanine aminotransferase, and aspartate aminotransferase levels decreased by 3.9%, 5.2%, and 16%, respectively, these changes were not statistically significant ( p > 0.05), suggesting preserved liver function without adverse effects. Histological evaluation revealed a significant reduction in microvesicular steatosis and IL‐6 immunoreactivity scores exclusively in the synbiotic group, indicating alleviated hepatic lipid accumulation and inflammation. Although synbiotic treatment did not alter overall gut microbiota diversity or species richness, it selectively enriched certain taxa, resulting in dominance of Coprococcus, Parabacteroides, and Bacteroides genera as identified by LEfSe analysis (LDA score ≥ 4, p < 0.05). Conversely, Streptococcus and [Ruminococcus] abundances significantly declined from 3.59% to 1.1% and 7.25% to 0.75%, respectively ( p < 0.05). Collectively, these findings demonstrate that synbiotic supplementation effectively improves lipid profiles and mitigates hepatic lipid accumulation and inflammation without compromising liver function. The modulation of specific gut microbiota taxa further supports its therapeutic potential. Therefore, the synbiotic formulation investigated herein represents a promising alternative biotherapeutic approach for managing hyperlipidemia.

The most common primary liver malignancy is hepatocellular carcinoma. Various chemotherapy drugs are used for treatment. These drugs have high toxicity to liver tissue. More effective, less toxic options should be preferred for treatment. The aim of this study is to investigate the cytotoxic effect of cisplatin and sodium vanadate combination (NaV) in hepatocellular carcinoma. The hepatocellular cancer cell line (HepG2) was used in this study. Increased concentration of cisplatin and a selected concentration of sodium vanadate were treated to HepG2 cells for 24- and 72-hours incubation times. The proliferation of HepG2 cells decreased with the combination of NaV and cisplatin. While cisplatin was effective in 10^–4 M concentration in the proliferation of HepG2 cells, 10^–4 M cisplatin with 10^–3 M NaV in combination was less effective in the proliferation of HepG2 cells. According to these results, NaV and cisplatin show toxic effects on hepatocellular carcinoma cells. However, the combination of cisplatin and NaV has a less toxic effect than cisplatin and NaV on hepatocellular carcinoma cells.