Aims. More than half of the patients with sepsis would develop cardiac dysfunction, which is termed as sepsis-induced myocardial dysfunction (SIMD). Previous studies suggest that autophagy may play an important role in SIMD. The present study investigated whether miR-214-3p could attenuate SIMD by inhibiting autophagy. Main Methods. In this article, we investigated the role of autophagy in a mouse model of cecal ligation and puncture (CLP). The structure and function of hearts harvested from the mice were evaluated. Myocardial autophagy levels were detected with immunohistochemical, immunofluorescent, and Western blot. Key Findings. miR-214-3p can alleviate SIMD in septic mice by inhibiting the level of cardiac autophagy to attenuate myocardial dysfunction. Moreover, this study showed that miR-214-3p inhibited autophagy by silencing PTEN expression in the myocardial tissues of septic mice. Significance. This study showed that miR-214-3p attenuated SIMD through myocardial autophagy inhibition by silencing PTEN expression and activating the AKT/mTOR pathway. The present findings supported that miR-214-3p may be a potential therapeutic target for SIMD.

The study's main objective was to investigate the effects of a specifi c blend of herbal extracts (HEs) on growth performance, antioxidant status, and components of the insulin-like growth factor (IGF) system in fi nishing pigs. A total of 16 PIC (Pig Improvement Company) pigs (60.1 ± 1.2 kg; eight gilts and eight barrows) were randomly assigned to one of the two dietary groups, with four pens/group (per pen: one gilt, one barrow). The pigs were fed with a basal diet containing 0 (control) or 250 mg HEs /kg diet for 47 days. The results indicated that herbal extract supplementation led to an increase (P<0.05) on the average daily gain and serum IGF-I level, and a decrease (P<0.05) on serum malondialdehyde and feed conversion ratio. However, feed intake was not affected (P>0.05). IGF-I, insulin receptor mRNA levels (liver, stomach, duodenum, muscle) and IGF-I receptor (IGF-IR) mRNA (stomach, duodenum, muscle) were high (P<0.05), while the level of IGF-IR mRNA was low (P<0.05) in the liver tissue compared with the control pigs. The results suggest that herbal extract supplementation has an antioxidant capacity, enhance the growth performance and exhibits tissue-specifi c regulation of IGF-IR mRNA level. In addition, the results also suggest the possible physiological role of the IGF system in controlling the HEs-supported growth of fi nishing pigs.

Previous studies have suggested that oxidative stress and autophagy results in acute kidney injury (aKi) during sepsis and microrna (mir)-214 serves a vital role in the protection of kidneys subjected to oxidative stress. The present study aimed to test whether the renoprotection of mir-214 is related to autophagy in sepsis. The role of autophagy was investigated in a mouse model of cecal ligation and puncture (clP). reverse transcription-quantitative polymerase chain reaction (rT-qPcr) was used to analyze the expression of mir-214. The structure and function of kidneys harvested from the mice were evaluated. Kidney autophagy levels were detected with immunohistochemical, immunofluorescent and western blotting. it was found that mir-214 could alleviate aKi in septic mice by inhibiting the level of kidney autophagy. Furthermore, mir-214 inhibited autophagy by silencing PTen expression in the kidney tissues of septic mice. These findings indicated that mir-214 ameliorated clP-induced aKi by reducing oxidative stress and inhibiting autophagy through the regulation of the PTen/aKT/mTor pathway.

Vitamin D deficiency is associated with acute myocardial infarction (AMI); thus we aimed to explore improvement effects of 1,25‐dihydroxyvitamin D3 (VD3) on the AMI and its potential mechanism. AMI models were constructed using male C57/BL6J mice and randomly treated with normal saline or VD3, using sham rats as control. Heart functions, myocardial damage, apoptosis, and inflammation were evaluated. Cardiomyocytes isolated from 3‐day‐old suckling mice were used for in vitro verification. After VD3 treatment, AMI‐induced cardiac dysfunction was reversed with better cardiac function parameters. VD3 treatment reduced inflammatory cell infiltration and myocardial infarction area accompanied by the reduction of inflammatory factors and myocardial infarction markers compared with the AMI group. VD3 treatment obviously alleviated AMI‐induced myocardial apoptosis, along with Bcl‐2 upregulation and downregulation of caspase‐3, caspase‐9, and Bax. Both in vivo and in vitro experiments revealed that VD3 enhanced the expression of LC3II and Beclin‐1 and decreased soluble p62. Furthermore, VD3 enhanced the AMI‐caused inhibition of PI3K, p‐AKT, and p‐mTOR expression, which was conversely reversed by the addition of 3‐methyladenine in vitro. The study highlights the improvement effects of VD3 on cardiac functions. We proposed a potential mechanism that VD3 protects against myocardial damage, inflammation, and apoptosis by promoting autophagy through PI3K/AKT/mTOR pathway.

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