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The incidence of depression has previously been correlated to hypertension. The aim of the present study was to explore the mechanisms of depression and hypertension by examining the expression and interaction of renin/prorenin receptor (PRR) and heme oxygenase 1 (HO-1) in vascular endothelial cells. A case-control study was conducted, and general data and serum factors were compared between hypertension patients complicated with depression and patients with hypertension alone. Logistic regression analysis was used to detect risk factors associated with hypertension complicated with depression. In addition, human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) and/or PRR gene silencing, and a Cell Counting Kit-8 (CCK-8) assay was performed to test their proliferation. The concentrations of inflammatory factors and oxidative stress factor were also detected using enzyme-linked immunosorbent assay and chemical colorimetry. Western blot analysis and reverse transcription-quantitative polymerase chain reaction were applied to detect protein and mRNA expression levels, respectively. The results revealed that HO-1 and renin precursor (Rep) were independent factors that affected hypertension complicated with depression. Serum HO-1 levels in patients with hypertension complicated with depression were significantly lower than that in hypertensive patients without depression, while Rep levels in patients with hypertension complicated with depression were significantly higher than that in hypertensive patients without depression. In HUVECs, ox-LDL reduced the cell proliferation in a dose-dependent manner, upregulated the expression of PRR gene and downregulated the expression of HO-1 gene. It was also observed that silencing of the PRR gene promoted the expression of the HO-1 gene. Furthermore, ox-LDL upregulated the inflammatory response and oxidative stress levels, while PRR gene silencing inhibited the ox-LDL-induced inflammatory factor and oxidative stress levels in HUVECs. Thus, regulating the expression levels of HO-1 and PRR to inhibit the oxidative stress and pro-inflammatory effect of ox-LDL may provide new insight for the treatment of hypertension patients with depression.

The present study aimed to evaluate the therapeutic effect of CO-releasing molecule-2 (CORM-2) in an established mouse orthotopic lung cancer model and investigate the underlying mechanism associated with inflammation pathway. A total of 80 mice were randomly divided into two groups with 20 serving as a normal control and 60 used for the orthotopic lung cancer model. The tumor group was either untreated, or administrated with DMSO or CORM-2. The mice were sacrificed at day 7 and 14 post-treatment, and the body weight, and thymus and spleen indices were determined. Pathological analysis was performed with hematoxylin and eosin (HE) staining. Serous inflammatory factors were measured using an ELISA. The expression levels of eukaryotic translation initiation factor 4E, p70S6K and toll-like receptor-4 (TLR4) were quantified by reverse transcription-polymerase chain reaction. The effects of CORM-2 on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), TLR4/nuclear factor (NF)-κB signaling pathways were determined by western blotting. The body weight increased over time in the control group, while it significantly declined in tumor-bearing mice (P