Objective To evaluate the efficacy of n-3 PUFAs (fish oil) for prevention of cardiovascular events. Methods Randomized controlled trials (RCTs) were searched from the following electronic databases: PubMed, EMbase, The Cochrane Library (Issue 1, 2009), CBM, and CNKI. Quality assessment and data extraction were conducted by two reviewers independently. Disagreement was resolved through discussion. All data were analyzed by using Review Manager 4.2 software. Results Five studies involving 37 689 participants met the inclusion criteria. Meta-analysis results showed that: 1) Compared with placebo, the incidence rates of the cardiovascular death (RR=0.91, 95% CI 0.84 to 0.98), cardiovascular events (RR=0.95, 95%CI 0.91 to 0.98), angina (RR=0.79, 95%CI 0.64 to 0.96), and myocardial infarction (RR=0.79, 95%CI 0.65 to 0.96) could be reduced by n-3 PUFAs (fish oil). 2) There were no significant differences in death from any cause, the hospitalization rates of cardiovascular disease, sudden death, and heart failure (RR=0.95, 95%CI 0.90 to 1.00; RR=0.97, 95%CI 0.93 to 1.02; RR=0.90, 95%CI 0.79 to 1.01; RR=0.98, 95%CI 0.91 to 1.06). 3) Compared with placebo, the incidence rates of the arrhythmia and stroke could be increased, but there were no significant differences (RR=1.14, 95%CI: 0.80 to 1.62; RR=1.12, 95%CI 0.97 to 1.30). Conclusion Compared with placebo, n-3 PUFAs (fish oil) has good effects on reducing the incidence rates of total cardiovascular events, cardiovascular death, myocardial infarction, and angina pectoris, and it has the same efficacy in death from all cause, sudden death, heart failure, and the hospitalization rates of cardiovascular disease. There are no significant differences in the increased rates of arrhythmia and stroke.
Diabetic retinopathy (DR) is one of the most common complications of diabetes mellitus (DM), and its pathogenesis remains incompletely understood. Research has identified inflammation as a key factor in the onset and progression of DR. As a group of systemic metabolic disorders, the dysregulation of polyunsaturated fatty acid (PUFA) metabolism induced by DM is closely related to the inflammatory mechanisms in DR. Recent metabolomic studies have revealed that in various stages of DR and in diabetic animal models, most upregulated PUFAs and their derivatives act as pro-inflammatory mediators, while downregulated PUFAs and their derivatives are predominantly anti-inflammatory. In the progression of DR, some PUFAs may exert anti-inflammatory effects by inhibiting microglial activation, reducing the expression of inflammatory proteins, antagonizing the pro-inflammatory effects of arachidonic acid, and suppressing the activation of inflammasomes and the migration of neutrophils. Conversely, other PUFAs may promote inflammation through mechanisms such as the formation of pro-inflammatory mediators resembling prostaglandins, facilitating leukocyte adhesion, and inducing oxidative stress responses. PUFAs play a complex dual role in the inflammatory mechanisms of DR. A deeper understanding of these mechanisms not only aids in elucidating the pathogenesis of DR but also provides potential targets for developing new therapeutic strategies.