The aim of this study was to evaluate the effect of c-aminobutyric acid (GABA) treatment on the enzymatic browning of fresh-cut potatoes. The browning index and activities of browning and defense-related enzymes were analyzed after 0, 1, 2, 3, 4, 5, and 6 days of storage at 4°C. The results showed that the treatment with 20 g/L GABA for 10 min significantly retarded the browning of fresh-cut potatoes. GABA inhibited the browning of freshcut potatoes by enhancing the activities of catalase and superoxide dismutase, and decreasing the activities of polyphenol oxidase and reactive oxygen species. The results suggest that GABA plays an important role in reducing the browning of fresh-cut potatoes. Hence, GABA treatment is a promising approach for reducing the browning and maintaining the quality of fresh-cut potatoes.
Gut bacterial translocation following impaired gut barrier is a critical determinant of initiating and aggravating acute pancreatitis (AP). Antibiotic combination (ABX; vancomycin, neomycin and polymyxin b) is capable of reducing gut bacteria, but its efficacy in AP prevention and the underlying mechanism have not been investigated yet. AP was induced in BALB/c mice by caerulein (CAE) hyperstimulation. We found that ABX supplementation attenuated the severity of AP as evidenced by reduced pancreatic oedema and myeloperoxidase activity. The protective effect was also confirmed by improved histological morphology of the pancreas and decreased pro-inflammatory markers (IL-1β, TNF-α, MCP-1) in pancreas. ABX administration inhibits the activation of colonic TLR4/NLRP3 inflammasome pathway. Subsequently, down-regulated NLRP3 resulted in decreased colonic pro-inflammation (IL-1β, IL-6, MCP-1) and enhanced gut physical barrier as evidenced by up-regulation of tight junction proteins including occludin, claudin-1 and ZO-1, as well as improved histological morphology of the colon. Together, combinatory ABX therapy inhibited the translocation of gut bacteria to pancreas and its amplification effects on pancreatic inflammation by inhibiting the pancreatic NLRP3 pathway, and inhibiting intestinal-pancreatic inflammatory responses. The current study provides the basis for potential clinical application of ABX in AP.
Background and Purpose: Despite recent advances in understanding its pathophysiology, treatment of acute kidney injury (AKI) remains a major unmet medical need, and novel therapeutic strategies are needed. Cathelicidin-related antimicrobial peptide (CRAMP) with immunomodulatory properties has an emerging role in various disease contexts. Here, we aimed to investigate the role of CRAMP and its underlying mechanisms in AKI. Experimental Approach: The human homologue LL-37 and CRAMP were measured in blood samples of AKI patients and in experimental AKI mice respectively. Experimental AKI was induced in wild-type and CRAMP-deficient (Cnlp −/− ) mice by ischaemia/reperfusion (I/R). Therapeutic evaluation of CRAMP was performed with exogenous CRAMP (5 mgÁkg −1 , i.p.) treatment. Key Results: Cathelicidin expression was inversely related to clinical signs in patients and down-regulated in renal I/R-induced injury in mice. Cnlp −/− mice exhibited exacerbated I/R-induced renal dysfunction, aggravated inflammatory responses and apoptosis. Moreover, over-activation of the NLRP3 inflammasome in Cnlp −/− mice was associated with I/R-induced renal injury. Exogenous CRAMP treatment markedly attenuated I/R-induced renal dysfunction, inflammatory response and apoptosis, correlated with modulation of immune cell infiltration and phenotype. Consistent with Cnlp −/− mouse data, CRAMP administration suppressed renal I/R-induced NLRP3 inflammasome activation, and its renal protective effects were mimicked by a specific NLRP3 inhibitor CY-09. The reno-protective and NLRP3 inhibitory effects of CRAMP required the EGF receptor.Conclusion and Implications: Our results suggest that CRAMP acts as a novel immunomodulatory mediator of AKI and modulation of CRAMP may represent a potential therapeutic strategy.Abbreviations: AG1478, inhibitor of EGFR; AKI, acute kidney injury; AMP, antimicrobial peptide; Cnlp −/− , CRAMP deficient; CRAMP, mouse cathelicidin-related antimicrobial peptide; E-cadherin, epithelial cadherin; I/R, ischaemia/reperfusion; LL-37, human cathelicidin; MPO, myeloperoxidase; NETs, neutrophil extracellular traps; NLRP3, nucleotide-binding domain leucine-rich repeat containing family, pyrin domain containing 3; PBS, phosphate buffer saline; RT-qPCR, real-time quantitative PCR; TUNEL, terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nickend labelling; WT, wild type.Li-Long Pan Wenjie Liang and Zhengnan Ren contributed equally to this work.
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