ABSTRACT
BACKGROUND: Colorectal cancer (CC) is the fourth most common type of cancer that causes illness and death. Medicines like ACE inhibitors and ARBs, usually used for heart problems, have shown they might help with the growth and development of CC. INTRODUCTION: An analysis of ACE inhibitors and colon cancer is conducted in this comprehensive review. The main goal is to see how ACEIs/ARBs affect the chances of getting cancer and dying in patients with CC. METHODS: A systematic literature search was conducted to identify relevant studies. Inclusion criteria encompassed studies that evaluated the use of ACEIs/ARBs in patients with CC and reported outcomes related to new cancer incidence and mortality. Data from selected studies were extracted and analyzed using appropriate statistical methods. RESULTS: The study showed that fewer cancer cases occurred in patients who took ACEIs/ARBs compared to those who did not (RR 0.962, 95% CI 0.934-0.991, p = 0.010). Furthermore, patients with CC who utilized ACEIs/ARBs exhibited a decreased mortality rate compared to non-users (HR 0.833, 95% CI 0.640-1.085, p = 0.175). CONCLUSION: This review suggests that using ACEIs/ARBs medicine could help people with CC live longer and lower their chances of dying. These results highlight the potential benefits of utilizing ACE inhibitors in the management of CC, warranting further investigation and consideration in clinical practice.
ABSTRACT
Protective effect of Qishen Yiqi dropping pills on the myocardium of rats with chronic heart failure (CHF) was investigated. Sixty rats were divided into the sham operation (n=20), the model (n=20) and the Qishen Yiqi dropping pill treatment group (n=20) using the random table method. The treatment group received administration of Qishen Yiqi dropping pills. The model and the sham operation group were given the same amount of normal saline. Within 24 h after the last administration, the rats were sacrificed. The myocardia were used for reverse transcription-polymerase chain reaction, western blot analysis and histological examination. In the sham operation group, cardiomyocytes were stained evenly and arranged neatly and densely with clear structures. In the model group, the cell morphology was fuzzy, the myocytes were hypertrophied, the nuclear pyknosis was fragmented, the arrangement was disordered, the intercellular space was narrowed, and the cytoplasm was missing. The apoptosis rates of cardiomyocytes in the model and Qishen Yiqi dropping pill treatment group were significantly higher than that in the sham operation group (P<0.05). The myocardial infarction areas in the model group and the Qishen Yiqi dropping pill treatment group were larger than that in the sham operation group (P<0.05). The expression levels of transforming growth factor-ß1, mothers against decapentaplegic homolog 2 (Smad2), Smad3, and caspase-3 messenger ribonucleic acids and proteins in the model group and the Qishen Yiqi dropping pill treatment group were higher than those in the sham operation group (P<0.05). Qishen Yiqi dropping pills have an obvious myocardial protective effect on CHF rats, which may enhance the degree of myocardial fibrosis by inhibiting the TGF-ß1/Smads pathway and improve cardiomyocyte apoptosis by suppressing the caspase-3 signaling pathway, thus protecting the myocardium.
ABSTRACT
The mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy.
