SET and MYND domain protein 2 (SMYD2) can methylate histone H3 at lysine36 (H3K36) and some non-histone substrates to play a role in tumorigenesis. However, It is unclear how SMYD2 contributes to chronic kidney disease (CKD). Here, AZ505 or LLY507, which could inhibit SMYD2, were used in cisplatin-induced CKD to investigate the effects and possible mechanisms by which they might act. We found that high expression of SMYD2 in cisplatin-induced CKD. However, AZ505 or LLY507 can significantly inhibit its expression, improve renal function injury and fibrosis induced by cisplatin, inhibit the transition of epithelial cells to a fibrogenic phenotype and fibrosis-related proteins, inhibit the expression of Inflammatory Cytokines (such as IL-6 and TNF-α), And inhibit the phosphorylation of pro-fibrosis molecule Smad3 and signal transduction and transcription activator-3 (STAT3) and up-regulated the expression of renal protective factor Smad7. In cultured tubular epithelial cells, AZ505 also can inhibit the expression of EMT, fibrosis-related proteins, and inflammatory cytokines in cisplatin-induced tubular epithelial cells. Based on these findings, SMYD2 may be a critical regulator of cisplatin-induced CKD and targeted pharmacological inhibition of SMYD2 may prevent cisplatin-induced CKD through Smad3 or STAT3-related signaling pathways.

Current diagnostic methods for diabetic nephropathy (DN) lack precision, especially in early stages and monitoring progression. This study aims to find potential biomarkers for DN progression and evaluate their accuracy. Using serum samples from healthy controls (NC), diabetic patients (DM), early-medium stage DN (DN-EM), and late-stage DN (DN-L), researchers employed quantitative proteomics and Mfuzz clustering analysis revealed 15 proteins showing increased expression during DN progression, hinting at their biomarker potential. Combining Mfuzz clustering with weighted gene co-expression network analysis (WGCNA) highlighted five candidates (HMGB1, CD44, FBLN1, PTPRG, and ADAMTSL4). HMGB1 emerged as a promising biomarker, closely correlated with renal function changes. Experimental validation supported HMGB1’s upregulation under high glucose conditions, reinforcing its potential as an early detection biomarker for DN. This research advances DN understanding and identifies five potential biomarkers, notably HMGB1, as a promising early monitoring target. These findings set the stage for future clinical diagnostic applications in DN.

The protein lysine methyltransferase 2 (SMYD2) can affect cell proliferation, differentiation, and survival through methylation of its histone and non‐histone substrates. SMYD2 has been shown to act as an oncogene to promote disease progression in a variety of cancer diseases, but its role in chronic kidney diseases (CKD) pathogenesis has not been fully elucidated. This study aims to investigate the effect of SMYD2 on cisplatin‐induced CKD and its underlying mechanisms. In this study, we found that cisplatin caused severe renal injury in mice, which was accompanied by the up‐regulation of SMYD2 expression. AZ505 treatment significantly down‐regulated cisplatin‐induced renal injury and fibrosis. It also alleviated renal apoptosis and inhibited the phosphorylation level of NF‐κB p65. Conditional knockdown of Smyd2 achieved similar effects as AZ505. In renal tubular epithelial cells, inhibition or silencing of SMYD2 down‐regulated cisplatin‐induced apoptotic response, while overexpression of SMYD2 induced apoptotic response and activated NF‐κB in response to the up‐regulation of SMYD2 expression. Up‐regulation of SMYD2 induced interaction and phosphorylation of SMYD2 and NF‐κB p65, and inhibition of NF‐κB activation further suppressed cisplatin‐induced NF‐κB activation and apoptosis. The present study suggests that up‐regulation of SMYD2 expression in cisplatin‐induced CKD may promote apoptosis of renal tubular epithelial cells and accelerate the process of renal injury through NF‐κB activation. SMYD2 may serve as a potential target for effective CKD treatment.

According to the special requirements of fresh agricultural products on temperature and humidity, a set of temperature and humidity monitoring system for low temperature fresh agricultural products was developed with ARM9 and ZigBee gateway as the core. The temperature and humidity of cold storage are controlled by microcomputer, and the data are collected. It realizes display and adaptive adjustment and alarm functions. A wireless sensor network based on 6 LoWPAN is proposed. The introduction of IPv6 in WSN ensures reliable data delivery. Practice has proved that the implementation of this project can not only effectively improve the information management of cold storage enterprises, but also promote the development of fresh agricultural supply chain enterprises from "storage type" to "logistics type".

Background: The study was designed to decipher the impact of platelet-rich plasma (PRP) on lipopolysaccharide (LPS)-mediated inflammation in BV2 (A murine cell line has been generated by infecting primary microglial cell cultures with a v-raf/v-myc oncogene carrying retrovirus (J2)) microglia. Method: BV2 microglia activation was induced by lipopolysaccharide (LPS) to establish an in vitro model of neuroinflammation. After pretreatment with different concentrations of PRP, the apoptosis of BV2 microglia was determined by flow cytometry, terminal deoxynucleotidyl transferase fluorescence labeling (TUNEL) and JC-1 assay. The production level of nitric oxide (NO) was determined by Griess method, and the mRNA (messenger RNA) expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX-2) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The contents of TNF-α, IL-1β, IL-6, and prostaglandin E2 (PGE2) cytokines were determined by enzyme-linked immunosorbent assay (ELISA). The phosphorylation of nuclear factor kappa-B (NF-κB/P65), inhibitor of NF-κB α (IκBα), c-Jun N-terminal kinase (JNK), extracellular signal-regulated MAP kinases 1/2 (ERK1/2), and p38 mitogen-activated protein kinases (p38 MAPKs) in the NF-κB/MAPKs pathway was analyzed by Western blot. The nuclear translocation of phosphorylated NF-κB/P65 subunits was evaluated by laser confocal microscopy. Results: PRP decreased LPS-stimulated apoptosis of BV2 microglia (p < 0.05). Moreover, PRP inhibited the mRNA levels of TNF-α, IL-1β, IL-6, iNOS, and COX-2 and the NO level (p < 0.05), in addition, PRP also reduced the production of inflammatory mediators including TNF-α, IL-1β, IL-6, and PGE2 (p < 0.05), inhibited the protein levels of p-NF-κB/P65, p-IκBα, p-JNK, p-ERK1/2, and p-p38 in the NF-κB/MAPKs pathway in LPS-induced BV2 microglia (p < 0.05), decreased the nuclear translocation of p-NF-κB/p65 subunit (p < 0.05). Particularly, PRP at a concentration of 10% showed the optimal the inhibition effects. Conclusions: PRP attenuates LPS-mediated inflammation in BV2 microglia by blocking the TLR4-NF-κB/MAPKs axis.

Cisplatin-induced nephrotoxicity remains a serious clinical complication that can progress to chronic kidney disease (CKD) and renal fibrosis. Partial epit