Understanding pathways from feeding difficulties of children to mental health risks of mothers at critical stages of childrearing: Does social support make a difference?

Background: Identifying the factors influencing mental health of mothers at critical stages of childrearing is significant for the implementation of effective promotion policies and counselling activities. Objective: This study aimed to investigate the relationships between children's feeding difficulties, marital quality, parenting quality and maternal mental health risks amidst Chinese mothers with high and low social support using a multi-group structural equation modelling approach. Participants: A cross-sectional study was conducted in Wenzhou, China and a total of 772 mothers with children aged 0-3 were surveyed by using purposive sampling. Findings: Results showed that of the 772 participants, 23.6 % reported anxiety, 50.1 % reported depression, 91.2 % reported insomnia, and 24 % reported feeding difficulties. The joint occurrence of multiple forms of mental problems is the most commonly reported features of mental health risks among mothers. The positive association between feeding difficulties of children and mental health risks of mothers was mediated by marital quality and parenting quality. In addition, feeding difficulties were not related to mental health risks in high social support group but all the relationships were significant in low social support group. Conclusions: These findings highlight the importance of the specific interventions to enhance social support, marital quality and parenting quality for improving mental health of mothers of children with feeding difficulties.

Bicyclol alleviates obesity-induced renal injury by inhibiting JNK and NF-κB-mediated inflammation.

Obesity is recognized as a major risk factor for chronic kidney disease (CKD), which is accompanied by increased renal lipid build-up, fibrosis, inflammation, apoptosis and pyroptosis. Bicyclol (BIC), a Chinese marketed hepatoprotective drug, has shown excellent anti-inflammatory, anti-fibrosis, anti-apoptotic, and lipid regulation effects in different animal models. In this study, we explored the role and mechanism of BIC in high-fat diet (HFD)-induced obesity-related nephropathy. Mice were fed with HFD for 24 weeks to develop obesity-related nephropathy, while mice in the BIC administration group were treated with BIC (50 mg/kg or 100 mg/kg, once every two days) at the last 12 weeks. We found that BIC treatment relieved the impairment of kidney structure and renal dysfunction caused by HFD. In addition, we found that BIC mitigated HFD-induced renal fibrosis, inflammation, apoptosis and pyroptosis by inhibiting JNK and NF-κB pathways. SV40-MES-13 cells treated with palmitate (PA) were used as the in vitro model. Our data show that BIC pre-administration relieved cellular damage caused by PA through suppressing JNK and NF-κB signaling pathways. In conclusion, we demonstrated that BIC attenuated obesity-induced renal injury by inhibiting chronic inflammation, fibrosis, apoptosis and pyroptosis via targeting JNK and NF-κB pathways. Our data suggested that BIC could be potentially used to prevent obesity-associated nephropathy, which warrants future investigation.

Toll-like receptor 2 deficiency ameliorates obesity-induced cardiomyopathy via inhibiting NF-κB signaling pathway.

Growing evidence demonstrates that chronic low-grade inflammation, which is induced by high-fat diet (HFD) or saturated fatty acid, plays an important role in the obesity-induced cardiomyopathy (OIC) process. Moreover, obesity is associated with the activation of different inflammatory pathways, including nuclear factor-κB (NF-κB), Toll-like-receptor-2 (TLR2) and Toll-like-receptor-4 (TLR4). In this study, we established an HFD-induced cardiac injury mouse model and palmitate (PA)-induced myocardial cell model to evaluate the role of TLR2 in OIC. Our data show that TLR2 blockade using TLR2 knockout (KO) mice or a TLR2-specific inhibitor, C29, markedly ameliorated HFD- or PA-induced inflammation, myocardial fibrosis, and hypertrophy both in vivo and in vitro. Moreover, the PA-induced myocardial cell injury was mediated via inducing the formation of TLR2-MyD88 complex in a TLR4-independent manner in cardiomyocytes. Our data prove the critical role of cardiac TLR2 in the pathogenesis of HFD- and saturated fatty acid-induced myocarditis, fibrosis, myocardial hypertrophy, and cardiac dysfunction. Inhibition of TLR2 pathway may be a therapeutic strategy of OIC.

Compound c17 alleviates inflammatory cardiomyopathy in streptozotocin-induced diabetic mice by targeting MyD88.

BACKGROUND: Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus and is associated with increased morbidity and mortality due to cardiac dysfunction. Chronic inflammation plays a significant role in the development of DCM, making it a promising target for novel pharmacological strategies. Our previous study has synthesized a novel compound, c17, which exhibited strong anti-inflammatory activity by specifically targeting to myeloid differentiation primary response 88 (MyD88). In this study, we evaluated the therapeutic effect of c17 in DCM. METHODS: The small molecular selective MyD88 inhibitor, c17, was used to evaluate the effect of MyD88 on DCM in both high concentration of glucose- and palmitic acid-stimulated macrophages and streptozotocin (STZ)-induced type 1 diabetes mellitus (T1DM) mice. RESULTS: The treatment of c17 in T1DM mice resulted in improved heart function and reduced cardiac hypertrophy, inflammation and fibrogenesis. RNA sequencing analysis of the heart tissues revealed that c17 effectively suppressed the inflammatory response by regulating the MyD88-dependent pathway. Co-immunoprecipitation experiments further confirmed that c17 disrupted the interaction between MyD88 and Toll-like receptor 4 (TLR4), consequently inhibiting downstream NF-κB activation. In vitro studies demonstrated that c17 exhibited similar anti-inflammatory activity by targeting MyD88 in macrophages, which are the primary regulators of cardiac inflammation. Furthermore, conditioned medium derived from c17-treated macrophages showed reduced capacity to induce hypertrophy, pro-fibrotic reactions, and secondary inflammation in cardiomyocytes. CONCLUSIONS: In conclusion, the small-molecule MyD88 inhibitor, c17, effectively combated the inflammatory DCM, therefore could be a potential candidate for the treatment of this disease.

Three Mental Health Symptoms of Frontline Medical Staff Associated With Occupational Stressors During the COVID-19 Peak Outbreak in China: The Mediation of Perceived Stress and the Moderation of Social Support.

The outbreak of COVID-19 epidemic has increased work demands for medical staff and has a certain impact on their mental health. The present study aimed to examine the role of perceived stress and social support in explaining the association between the occupational stressors and three mental health symptoms (i.e., anxiety, depression, and insomnia) of frontline medical staff. Five hundred twenty five frontline medical staff were investigated online after the outbreak of the COVID-19 (16 February, 2020-2 March, 2020) in China. The results found that the prevalence of anxiety, depression, and insomnia among frontline medical staff were 39.8, 29.9, and 37.9%, respectively. Occupational stressors were associated with anxiety, depression, and insomnia symptoms. Perceived stress significantly mediated this link. Social support moderated the second half of the indirect effect of occupational stressors on anxiety and depression symptoms. Under the epidemic situation of COVID-19, for frontline medical staff, high perceived stress and low social support may increase vulnerability for mental health symptoms triggered by occupational stressors. Thus, improving the social support and promoting the cognitive reappraisal of perceived stress may help to maintain mental health among medical staff.