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Hypertension-induced ventricular and vascular remodeling causes myocardial infarction, heart failure, and sudden death. Most available pharmaceutical products used to treat hypertension lead to adverse effects on human health. Limited data is available on apitherapy (bee products) combinations for treatment of hypertension. This study aims to evaluate the antihypertensive effects of combinations of natural apitherapy compounds used in the medical sector to treat a variety of diseases. Rats were assigned into six groups consisting of one control group and five hypertensive groups where hypertension (blood pressure > 140/90) was induced with dexamethasone. One of these groups was used as a hypertension model, while the remaining four hypertensive groups were treated with a propolis, royal jelly, and bee venom combination (PRV) at daily oral doses of 0.5, 1.0, and 2.0 mg/kg, and with losartan 10 mg/kg. The PRV combination at all doses decreased arterial blood pressure below the suboptimal value (p < 0.001), and PRV combination treatment improved dexamethasone-induced-ECG changes. The same treatment decreased angiotensin-II, endothelin-1, and tumor growth factor β serum levels in hypertensive rats. Additionally, PRV combination improved histopathological structure, and decreased serum levels of NF-kB and oxidative stress biomarkers. We concluded that PRV combination therapy may be used as a potential treatment for a variety of cardiovascular diseases.

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Hepatocellular carcinoma (HCC) is a fatal disease, accounting for 75–85% of primary liver cancers. The conclusive research on miR-181c-5p’s role in hepatocarcinogenesis, whether it has oncogenic effects or acts as a tumor repressor, is limited and fluctuating. Therefore, the current study aimed to elucidate the role of miR-181c-5p in HCC in silico and in vivo. The bioinformatics analysis of miR-181c-5p expression data in HCC using several databases strongly shed light on its involvement in HCC development, but also confirmed the fluctuating data around its role. miR-181c-5p was proven here to have an oncogenic role by increasing HepG2 cells’ viability as confirmed by MTT analysis. In addition, miR-181c-5p was upregulated in the HCC positive control group and progressed the HCC development and malignant features by its forced expression in an HCC mouse model by targeted delivery using a LA-PAMAM polyplex. This is indicated by the cancerous gross and histological features, and the significant increase in liver function biomarkers. The functional enrichment bioinformatics analyses of miR-181c-5p-downregulated targets in HCC indicated that miR-181c-5p targets were significantly enriched in multiple pathways and biological processes involved in HCC development. Fbxl3, an example for miR-181c-5p potential targets, downregulation and its correlation with miR-181c-5p were validated by qPCR. In conclusion, miR-181c-5p is upregulated in HCC and has an oncogenic role enhancing HCC progression.

No abstract