Could early life DHA supplementation benefit neurodevelopment? A systematic review and meta-analysis.

Background: Docosahexaenoic acid (DHA) plays a crucial role in the growth and functional development of the infant brain. However, the impact of additional DHA supplementation on neurodevelopment in infants remains controversial in randomized controlled trials. In this systematic review and meta-analysis, we aimed to investigate the effects of prenatal and postnatal DHA supplementation on neurodevelopment. Methods: We systematically searched the MEDLINE, EMBASE, and Cochrane Library electronic databases using a predefined strategy until 8 February 2024. We extracted relevant study characteristics and outcomes related to the nervous system. Two independent reviewers critically evaluated the included studies to assess their validity and risk of bias. Results: A total of 21 studies met our inclusion criteria, one study was removed after quality assessment, and the meta-analysis included 9 randomized controlled trials. The meta-analysis results indicated that there was no statistically significant difference between the DHA supplementation group and the placebo group, as assessed by the Mental Development Index [MDI; mean difference (MD), 0.41; 95% confidence interval (CI), -0.91 to 1.73; p = 0.55]. However, the DHA group had a significantly higher Psychomotor Development Index (PDI) than the placebo group (MD, 1.47; 95% CI, 0.23 to 2.72; p = 0.02). Subgroup analyses based on populations showed that DHA supplementation was superior to placebo for infants in both MDI (language score conversion; MD, 2.05; 95% CI, -0.16 to 4.26; p = 0.07) and PDI (MD, 1.94; 95% CI, 0.23 to 3.65; p = 0.03). Other subgroup analyses indicated no statistical differences between the two groups. The remaining assessments that could not be summarized quantitatively underwent a narrative evaluation. Conclusion: Based on the BSID assessments, DHA supplementation in infants may have potential neurodevelopmental benefits. Because the meta-analysis included few high-quality articles and had some limitations, more relevant articles are needed to address the need for separate DHA supplementation in infants, pregnant women, and lactating mothers. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022348100, identifier: CRD42022348100.

Green tea extract catechin improves internal cardiac muscle relaxation in RCM mice.

BACKGROUND: Diastolic dysfunction refers to an impaired relaxation and an abnormality in a heart's filling during diastole while left ventricular systolic function is preserved. Diastolic dysfunction is commonly observed in patients with primary hypertension, diabetes and cardiomyopathies such as hypertrophic cardiomyopathy or restrictive cardiomyopathy. We have generated a restrictive cardiomyopathy (RCM) mouse model with troponin mutations in the heart to mimic the human RCM patients carrying the same mutations. RESULTS: In the present study, we have investigated the ventricular muscle internal dynamics and pressure developed during systole and diastole by inserting a micro-catheter into the left ventricle of the RCM mice with or without treatment of desensitizer green tea extracts catechins. Our results demonstrate that green tea catechin is able to correct diastolic dysfunction in RCM mainly by improving ventricular compliance and reducing the internal muscle rigidity caused by myofibril hypersensitivity to Ca(2+). CONCLUSION: Green tea extract catechin is effective in correcting diastolic dysfunction and improving ventricular muscle intrinsic compliance in RCM caused by troponin mutations.

Antithetical regulation of α-myosin heavy chain between fetal and adult heart failure though shuttling of HDAC5 regulating YY-1 function.

Molecular switches of myosin isoforms are known to occur in various conditions. Here, we demonstrated the result from fetal heart failure and its potential mechanisms. Fetal and adult heart failure rat models were induced by injections of isoproterenol as previously described, and Go6976 was given to heart failing fetuses. Real-time PCR and Western blot were adopted to measure the expressions of α-MHC, ß-MHC and YY-1. Co-immunoprecipitation was performed to analysis whether YY-1 interacts with HDAC5. Besides, histological immunofluorescence assessment was carried out to identify the location of HDAC5. α-MHC was recorded elevated in fetal heart failure which was decreased in adult heart failure. Besides, YY-1 was observed elevated both in fetal and adult failing hearts, but YY-1 could co-immunoprecipitation with HDAC5 only in adult hearts. Nuclear localization of HDAC5 was identified in adult cardiomyocytes, while cytoplasmic localization was identified in fetuses. After Go6976 supplied, HDAC5 shuttled into nucleuses interacted with YY-1. The myosin molecular switches were reversed with worsening cardiac functions and higher mortalities. Regulation of MHC in fetal heart failure was different from adult which provided a better compensation with increased α-MHC. This kind of transition was involved with shuttling of HDAC5 regulating YY-1 function.

Evaluation of oxidative stress in placenta of fetal cardiac dysfunction rat model and antioxidant defenses of maternal vitamin C supplementation with the impacts on P-glycoprotein.

AIM: The oxidative stress of placenta during fetal heart dysfunction (FHD) is lack of evaluation. So, we carried out an experiment to explore whether vitamin C (VitC) can be supplied for placental protection under FHD and its impacts on P-glycoprotein expression. METHODS: Fetal heart dysfunction was induced by two intra-amniotic injections of isoproterenol, then (VitC) was supplied. Hematoxylin-eosin (HE) staining was used to evaluate placental histology, and oxidative stress was measured by total antioxidant capacity, total superoxide dismutase and level of advanced oxidation protein products (AOPP), as well as apoptosis rate. Real-time polymerase chain reaction was adopted to measure the expressions of superoxide dismutase-1 (Sod-1), glutathione peroxidase-1 (Gpx-1) and endothelial nitric oxide synthase (eNOS) in placenta. Finally, western blot was performed to detect P-glycoprotein expression. RESULTS: All isoproterenol twice-treated fetuses exhibited significant (P < 0.05) contractile dysfunction by fetal echocardiography compared to others. The HE staining showed severe placental hydrops in the FHD group, and that hydrops could be reduced by VitC treatment. Total antioxidant capacity and total Sod-1 decreased in FHD and elevated after VitC supplementation. Also, level of AOPP increased in FHD and dropped after VitC supplementation. Analysis of apoptosis demonstrated that there was a mild increase in apoptosis rate of FHD. Reductions of Sod-1 and eNOS mRNA expression were confirmed in FHD, but these could recovered after VitC supplementation, with the same tendency of the P-glycoprotein. CONCLUSION: Severe oxidative injuries were identified in placentas of FHD with P-glycoprotein repression. VitC administration can reduce the oxidative stress and rebuild the protective mechanism of placenta.