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Poly(lactic-glycolic acid) (PLGA) is a biocompatible bio-scaffold material, but its own hydrophobic and electrically neutral surface limits its application as a cell scaffold. Polymer materials, mimics ECM materials, and organic material have often been used as coating materials for PLGA cell scaffolds to improve the poor cell adhesion of PLGA and enhance tissue adaptation. These coating materials can be modified on the PLGA surface via simple physical or chemical methods, and coating multiple materials can simultaneously confer different functions to the PLGA scaffold; not only does this ensure stronger cell adhesion but it also modulates cell behavior and function. This approach to coating could facilitate the production of more PLGA-based cell scaffolds. This review focuses on the PLGA surface-modified materials, methods, and applications, and will provide guidance for PLGA surface modification.

Background: Depression is a common and potentially life-threatening mental illness, and currently, there is a lack of effective treatment. It has been reported that dehydrocorydaline (DHC) can inhibit monoamine transporter uptake in depressed CUMS mice, but more possible mechanisms of action remain to be further studied.Methods: C57BL/6 mice were exposed to chronic unpredictable mild stress (CUMS) for five consecutive weeks. The mice were administrated with dehydrocorydaline or fluoxetine (FLU) for four consecutive weeks. Behavioral tests including sucrose preference test (SPT), tail suspension test (TST), and forced swimming test (FST) were applied. In parallel, hematoxylin and eosin (H&E) staining and Nissl staining were used to explore the effect of DHC on pathological changes in the hippocampus. The concentrations of depression-related factors (5-HT and DA) and inflammatory factors (TNF-α, IL-6, and IL-1β) in the hippocampus and serum were assessed by ELISA assay. NLRP3 inflammasome pathway-related proteins (NLRP3, IL-18, IL-1 IL-1α, and caspase-1) were detected by western blot. The activation of microglia and astrocytes was subjected to immunofluorescent staining. Additionally, microglia were treated with DHC (100 mg/L) for 24 h following incubation with 100 ng/ml LPS for 12 h. ov-NC or ov-NLRP3 plasmid was transfected into microglia 6 h before LPS induction for exploring the effect of NLRP3 overexpression on DHC-inhibited microglia activation. Then, conditioned media of microglia were collected from each group, followed by intervention of astrocytes for 24 h to explore the effect of NLRP3 overexpression of microglia on astrocyte activation.Results:In vivo administration of DHC was found to ameliorate depressive-like behaviors and attenuate neuron damage of CUMS mice. DHC increased neurotransmitter concentration, reduced the proinflammatory factor levels, attenuated NLRP3 inflammasome activation, and decreased A1 astrocyte and microglia activation in the hippocampus of CUMS mice. Furthermore, in vivo results showed that activated microglia induced activation of A1 astrocytes but not A2 astrocytes.Conclusion: Taken together, we provided evidence that DHC exhibited antidepressive effects on CUMS mice possibly via NLRP3 inflammasome-mediated astrocyte activation.

Background: Primary insomnia (PI) is one of the most common complaints among the general population. Both non-pharmacological and pharmacological therapies have proven effective in treating primary insomnia. However, the underlying mechanism of treatment remains unclear, and no studies have compared the underlying mechanisms of different treatments. Methods: In this study, we investigated gray matter volume (GMV) and resting-state functional connectivity (rsFC) changes following both pharmacological and non-pharmacological treatments in patients with PI. A total of 67 PI patients were randomized into benzodiazepine treatment, cupping treatment, or a wait-list control group for 4 weeks. The Pittsburgh Sleep Quality Index (PSQI), gray matter volume (GMV), and resting-state functional connectivity (rsFC) of the hippocampus were measured at the beginning and end of the experiment. Results: We found 1) significantly decreased PSQI scores in the cupping and benzodiazepine treatment groups compared to the control group with no significant differences between the two treatment groups; 2) significant GMV increases in the cupping group compared to the control group at the right hippocampus after 4 weeks of treatment; 3) significantly increased rsFC between the right hippocampus and left rostral anterior cingulate cortex/medial prefrontal cortex (rACC/mPFC) in the two treatment groups, which was significantly associated with PSQI score decreases. Discussion: Our findings suggest that benzodiazepine and cupping may share a common mechanism to relieve the symptoms of patients with PI. Keywords: Primary insomnia, Hippocampus, Non-pharmacological therapy, Pharmacological therapy, Gray matter volume, Resting-state functional connectivity

This study was conducted to investigate potential regulatory mechanisms of feed efficiency (FE) in sheep by linking rumen microbiota with its host by the multi-omics analysis. One hundred and ninety-eight hybrid female sheep (initial body weight = 30.88 ± 4.57 kg; 4-month-old) were selected as candidate sheep. Each test sheep was fed in an individual pen for 60 days, and the residual feed intake (RFI) was calculated. The ten candidate sheep with the highest RFI were divided into the Low-FE group, and the ten with the lowest RFI were divided into the High-FE group, all selected for sample collection. The RFI, average daily gain and average daily feed intake were highly significantly different between the two experimental groups (P

ABSTRACTTransplant of donor microbiota can significantly alter the structure of the host’s intestinal microbiota and alleviate early weaning stress. Screening for alternative-resistant products by transplanting fecal bacteria from healthy lambs is a current research trend in the livestock industry. In the present study, fecal microbiota transplantation was performed in lambs with diarrhea during early weaning. The transplanted fecal microbiota greatly reduced the diarrhea and serum inflammatory factor levels caused by early weaning. Transcriptome sequencing revealed that fecal microbiota transplantation alleviated colonic inflammation and increased the expression of colonic ion transport proteins. In addition, the levels of Streptococcus, Enterococcus, and Escherichia Shigella decreased in the jejunum, cecum, and colon of the lambs; meanwhile, the levels of Bifidobacterium and multiple secondary bile acids, such as ursodeoxycholic acid, increased in the colon. Furthermore, the abundance of Bifidobacterium was significantly negatively correlated with the diarrhea index. The fecal microbiota transplantation reshaped the intestinal microbiota of early-weaned lambs, protected the intestinal physiology and immune barrier, and reduced weaning stress. In addition to making available bacteriological products for controlling intestinal inflammation in young lambs, this study offers a theoretical framework and technical system for the mechanisms by which microbiota transplantation regulates intestinal health in young lambs.IMPORTANCEBefore weaning, the digestive system of lambs is not well developed; hence, its resistance to infectious diseases is weak. Under intensive feeding systems, lambs can easily be stressed and the risk of bacterial infection is high, which causes diarrhea, which in turn may cause mortality and significant economic losses to the livestock industry. With the elimination of antibiotics in animal feed, the incidence of mortality due to intestinal illnesses in lambs has gradually increased. There are several types of probiotics routinely used in young animals, but the effects and processes of their usage have only been assessed in monogastric animals. The lack of data on ruminants, particularly sheep, has severely hampered the process of efficient and healthy sheep breeding. Therefore, there is an urgent need to identify effective and safe functional supplements for lambs.

Abstract Objective This study aimed to investigate the mechanism by which Chinese herbal medicine ulcer oil (UO) accelerates ulcer healing in a diabetic ulcer rat model. Methods Sprague Dawley rats were allocated at random into four groups: a control group, a positive control group (PC), a UO treatment group and an ethacridine lactate solution treatment group. Subcutaneous tissue was surgically removed from the rats on days 3, 7 and 14. The levels of protein phosphotyrosine phosphatase 1B (PTP1B), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF) and advanced glycation end products (AGEs) were detected using western blot analysis. Results PTP1B protein expression was significantly lower in the UO group compared with the PC group. VEGF protein expression was significantly higher in the UO group than in the control group on day 3. PDGF protein expression in the UO group was significantly higher than in the PC group on day 3. AGE expression was significantly lower in the UO group than in the PC group. Conclusions UO may downregulate PTP1B and AGEs and upregulate VEGF and PDGF, which may contribute to the inhibition of the inflammatory response and promote the healing of diabetic foot ulcers.