Global trends in oxidative stress in the Retina: A bibliometric analysis of 2013-2023.

Background: Oxidative stress plays a significant role in the pathogenesis of many retinal diseases. However, only a few systematic bibliometric studies have been conducted. This study aims to visualize research hotspots and developmental trends in oxidative stress in the retina from 2013 to 2023 by analyzing bibliometric data. Methods: We retrieved papers on oxidative stress in the retina published between 2013 and 2023 from the Web of Science Core Collection. The data were visually analyzed using CiteSpace and VOSviewer software. Results: The total number of 2100 publications were included in the analysis. An overall increasing trend in the number of publications is observed between 2013 and 2023. Chinese publications were the most contributive, but United States publications were the most influential. Shanghai Jiao Tong University was the most active and prolific institution. Antioxidants was the most productive journal, while Oxidative Medicine and Cellular Longevity were the journals with the most-cited articles. Kaarniranta K, from Finland, was the most productive and influential author. Examination of co-cited references revealed that researchers in the field are primarily focused on investigating the molecular mechanisms, preventive strategies, and utilization of antioxidants to address retinal oxidative damage. Diabetic retinopathy, endothelial growth factor, retinitis pigmentosa, retinal degeneration, antioxidant response, retinal ganglion cells, and genes are the research hotspots in this field. Metabolism, sodium iodate, and system are at the forefront of research in this field. Conclusion: Attention toward retinal oxidative stress has increased over the past decade. Current research focuses on the mechanisms of retinal diseases related to oxidative stress and the experimental study of antioxidants in retinal diseases, which may continue to be a trend in the future.

Atractylenolide I Alleviates Indomethacin-Induced Gastric Ulcers in Rats by Inhibiting NLRP3 Inflammasome Activation.

Atractylodes macrocephala Koidz, a traditional Chinese medicine, contains atractylenolide I (ATR-I), which has potential anticancer, anti-inflammatory, and immune-modulating properties. This study evaluated the therapeutic potential of ATR-I for indomethacin (IND)-induced gastric mucosal lesions and its underlying mechanisms. Noticeable improvements were observed in the histological morphology and ultrastructures of the rat gastric mucosa after ATR-I treatment. There was improved blood flow, a significant decrease in the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1ß, and IL-18, and a marked increase in prostaglandin E2 (PGE2) expression in ATR-I-treated rats. Furthermore, there was a significant decrease in the mRNA and protein expression levels of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), cysteinyl aspartate specific proteinase-1 (caspase-1), and nuclear factor-κB (NF-κB) in rats treated with ATR-I. The results show that ATR-I inhibits the NLRP3 inflammasome signaling pathway and effectively alleviates local inflammation, thereby improving the therapeutic outcomes against IND-induced gastric ulcers in rats.

Astragaloside IV ameliorates indomethacin-induced intestinal inflammation in rats through inhibiting the activation of NLRP3 inflammasome.

The administration of nonsteroidal anti-inflammatory drugs (NSAIDs) may cause significant intestinal alteration and inflammation and lead to the occurrence of inflammatory diseases resembling duodenal ulcers. Astragaloside IV (AS-IV) is a glycoside of cycloartane-type triterpene isolated from the dried root of Astragalus membranaceus (Fisch.) Bge. (family Fabaceae), and has been used for ameliorating the NSAID-induced inflammation in the small intestine. The present study aimed to investigate the effects of AS-IV on indomethacin (IND)-induced inflammation in the small intestine of rats and its underlying mechanisms. Hematoxylin-eosin (H&E) staining, transmission and scanning electron microscopy were carried out to observe the surface morphology and ultrastructure of the small intestinal mucosa. Immunofluorescence and ELISA tests were employed to detect the expressions of NLRP3, ASC, caspase-1, and NF-κB proteins, as well as inflammatory factors IL-1ß and IL-18, to uncover potential molecular mechanisms responsible for mitigating small intestinal inflammation. The results demonstrated that AS-IV significantly decreased the ulcer index, improved the surface morphology and microstructure of the small intestinal mucosa, and increased mucosal blood flow. Molecular docking revealed a strong and stable binding capacity of AS-IV to NLRP3, ASC, caspase-1, and NF-κB proteins. Further experimental validation exhibited that AS-IV markedly decreased levels of IL-1ß and IL-18, and inhibited the protein expression of NLRP3, ASC, caspase-1, and NF-κB. Our data demonstrate that AS-IV ameliorates IND-induced intestinal inflammation in rats by inhibiting the activation of NLRP3 inflammasome and reducing the release of IL-1ß and IL-18, thereby representing a promising therapy for IND-induced intestinal inflammation.

Global knowledge mapping and emerging trends in Helicobacter pylori-related precancerous lesions of gastric cancer research: A bibliometric analysis from 2013 to 2023.

Helicobacter pylori (H pylori) infection is a crucial element in chronic gastritis progression towards precancerous lesions of gastric cancer (PLGC) formation and, potentially, gastric cancer; however, screening for and eliminating H pylori has several challenges. This study aimed to assess the present research status, prominent themes, and frontiers of H pylori-related PLGC and to provide impartial evaluations of the developmental trends in this domain. This study extracted articles and review papers concerning H pylori-related PLGC published from 2013 to 2023 from the Web of Science Core Collection. The data was analyzed and visualized using VOSviewer and CiteSpace. The study encompassed 1426 papers, with a discernible upward trend in publications between 2013 and 2023. China emerged as the most productive country, whereas the United States exerted the greatest influence. Baylor College of Medicine was the most prolific institution. World Journal of Gastroenterology featured the highest number of published papers, whereas Gastroenterology was the most frequently cited journal. Kim N. from South Korea was the most prolific author. Co-cited literature pertained to various aspects such as gastritis classification, H pylori infection management, gastric cancer prevention, and managing patients with PLGC. Future research will focus on the Kyoto classification, cancer incidence, and gastric intestinal metaplasia. The results of this study indicate a persistent increase in attention directed toward H pylori-associated PLGC. The research emphasis has transitioned from molecular mechanisms, epidemiology, monitoring, and diagnosis to clinical prevention and treatment methodologies. The forthcoming research direction in this area will concentrate on controlling and preventing malignant PLGC transformation.

Epigenetics: Novel crucial approach for osteogenesis of mesenchymal stem cells.

Bone has a robust regenerative potential, but its capacity to repair critical-sized bone defects is limited. In recent years, stem cells have attracted significant interest for their potential in tissue engineering. Applying mesenchymal stem cells (MSCs) for enhancing bone regeneration is a promising therapeutic strategy. However, maintaining optimal cell efficacy or viability of MSCs is limited by several factors. Epigenetic modification can cause changes in gene expression levels without changing its sequence, mainly including nucleic acids methylation, histone modification, and non-coding RNAs. This modification is believed to be one of the determinants of MSCs fate and differentiation. Understanding the epigenetic modification of MSCs can improve the activity and function of stem cells. This review summarizes recent advances in the epigenetic mechanisms of MSCs differentiation into osteoblast lineages. We expound that epigenetic modification of MSCs can be harnessed to treat bone defects and promote bone regeneration, providing potential therapeutic targets for bone-related diseases.

The Role of Catechins in Regulating Diabetes: An Update Review.

Catechins are key functional components in tea and have many health benefits, including relieving diabetes. Glucose is necessary for maintaining life. However, when the glucose in the serum exceeds the threshold, it will lead to hyperglycemia. Hyperglycemia is mainly caused by insufficient insulin secretion or insulin resistance. Persistent hyperglycemia can cause various disorders, including retinopathy, nephropathy, neurodegenerative diseases, cardiovascular disease, and diabetes. In this paper, we summarize the research on the underlying mechanisms of catechins in regulating diabetes and elaborate on the mechanisms of catechins in alleviating hyperglycemia by improving insulin resistance, alleviating oxidative stress, regulating mitochondrial function, alleviating endoplasmic reticulum stress, producing anti-inflammatory effects, reducing blood sugar source, and regulating intestinal function. This review will provide scientific direction for future research on catechin alleviating diabetes.

Traditional Chinese Medicine prescription Huang-Qi-Jian-Zhong-Tang ameliorates indomethacin-induced duodenal ulcers in rats by affecting NF-κB and STAT signaling pathways.

Huang-Qi-Jian-Zhong-Tang (HQJZT) is a well-known traditional Chinese herbal formulation. This study aimed to investigate the duodenoprotective properties of HQJZT against Indomethacin (IND)-induced duodenal ulceration in rats, and the mechanisms involved, particularly through NF-κB and STAT signaling pathways. Our results showed that HQJZT completely protected the duodenal mucosa from ulceration caused by IND, as indicated by improved macroscopic and histological appearances. There was a significant decrease in ulcer index and microscopic score, an increase in villus height and crypt depth, and a normalization of the tissue architecture of the duodenum in rats following HQJZT treatment. Blood flow into the duodenal mucosa was significantly increased after HQJZT administration. HQJZT significantly increased PGE2 and NO levels in the duodenal mucosa. A significant reduction in the production of pro-inflammatory cytokines IL-1ß, IL-6, and TNF-α was observed in the duodenal mucosa under treatment with HQJZT. Mechanistically, the administration of HQJZT significantly lowered the duodenal protein expression of inflammation-related genes, including p-NF-κB and p-IκBß, compared with the ulcer control group. Furthermore, the STAT signaling pathway-related protein markers p-JAK and p-STAT were significantly reduced in the HQJZT (1.30 and 2.60 g/kg) groups. As a result of these findings, HQJZT alleviates duodenal mucosal ulcers caused by IND. A protective effect of HQJZT on duodenal ulcers is attributed to its ability to improve mucosal blood flow, stimulate the production of cytoprotective mediators, minimize proinflammatory cytokines, and block the activation of NF-κB and STAT signaling pathways.

C1r and C1s from Nile tilapia (Oreochromis niloticus): Molecular characterization, transcriptional profiling upon bacterial and IFN-γ inductions and potential role in response to bacterial infection.

The complement components C1r and C1s play a vital role in immunity with the activation of C1 complex in the classical complement pathway against pathogen infection. In this study, Nile tilapia (Oreochromis niloticus) C1r and C1s orthologs (OnC1r and OnC1s) were identified and characterized. The cDNA of OnC1r and OnC1s ORFs consisted of 1902 bp and 2100 bp of nucleotide sequence encoding polypeptides of 633 and 699 amino acids, respectively. The deduced OnC1r and OnC1s proteins both possessed CUB, EGF, CCP and SP domains, which were significantly homology to teleost. Spatial mRNA expression analysis revealed that the OnC1r and OnC1s were highly expressed in liver. After the in vivo challenges of Streptococcus agalactiae (S. agalactiae) and lipopolysaccharide (LPS), the mRNA expressions of OnC1r and OnC1s were significantly up-regulated in liver and spleen, which were consistent with immunohistochemical detection at the protein level. The up-regulation of OnC1r and OnC1s expressions were also demonstrated in head kidney monocytes/macrophages in vitro stimulated with LPS, S. agalactiae, and recombinant OnIFN-γ. Taken together, the results of this study indicated that OnC1r and OnC1s were likely to get involved in the immune response of Nile tilapia against bacterial infection.