RETRACTED: Tangzhiqing-mediated NRF2 reduces autophagy-dependent ferroptosis to mitigate diabetes-related cognitive impairment neuronal damage.

The publisher of Rejuvenation Research officially retracts the article entitled, "Tangzhiqing-mediated NRF2 reduces autophagy-dependent ferroptosis to mitigate diabetes-related cognitive impairment neuronal damage," by Lingyan Qiu, Mr. Kai Chen, Prof. Xu Wang, and Ms. Yun Zhao. (Rejuvenation Res 2023; epub 6 Jun; doi: 10.1089/rej.2023.0013). After the acceptance and Instant Online publication of the paper, the authors were contacted repeatedly regarding their page proofs, and for further clarification of unresolved issues within the paper. All attempts to reach the authors were unsuccessful. Concurrently, the publisher identified a problematic overlap with a paper published in 2023 in Endocrine, Metabolic & Immune Disorders - Drug Targets.1 This paper was subsequently withdrawn. These troubling details have led the editorial leadership of Rejuvenation Research to lose confidence in the validity of the submission and to retract the paper. All authors were notified of the decision to retract the paper via email. The lead author, Lingyan Qiu, and the corresponding author, Xu Wang, quickly responded and appealed the decision to retract. The appeal was denied. Reference 1. https://www.eurekaselect.com/article/132631. Withdrawn: Experimental study on NRF2 mediated by Chinese medicine tangzhiqing to reduce autophagy-dependent ferroptosis and alleviate neuron damage in HT22 mice with diabetes-related cognitive disorder. 22 June, 2023; DOI: 10.2174/1871530323666230622151649 Diabetes is a chronic condition defined by the body's inability to process glucose. The most common form, diabetes mellitus, reflects the body's insulin resistance, which leads to long-term raised glucose blood levels. These levels can cause oxidative damage, cell stress, and excessive autophagy throughout the body, including the nervous system. Diabetes-related cognitive impairment (DCI) results from chronic elevation of blood glucose, and as diabetes cases continue to rise, so too do comorbidities such as DCI. Although there are medications to address high blood glucose, there are few that can inhibit excessive autophagy and cell death. Therefore, we investigated if the Traditional Chinese Medicine, Tangzhiqing (TZQ), can reduce the impact of DCI in a high-glucose cell model. We used commercially available kits to evaluate cell viability, mitochondrial activity, and oxidative stress. We found that TZQ treatment increased cell viability, ensured continued mitochondrial activity, and reduced reactive oxygen species. We also found that TZQ functions by increasing NRF2 activity, which decreases the ferroptotic-associated pathways that involve p62, HO-1, and GPX4. Therefore, TZQ should be further investigated for its role in reducing DCI.

Withdrawn: Experimental Study on NRF2 Mediated by Chinese Medicine Tangzhiqing to Reduce Autophagy-dependent Ferroptosis and Alleviate Neuron Damage in HT22 Mice with Diabetes-related Cognitive Disorder

The article has been withdrawn at the request of the authors of the journal Endocrine, Metabolic & Immune Disorders-Drug Targets.Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php. BENTHAM SCIENCE DISCLAIMER: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultane-ously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submit-ting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Gua Lou Er Chen decoction attenuates atherosclerosis by reducing proteoglycans accumulation and inflammation.

BACKGROUND: Proteoglycans (PGs) accumulation and inflammation are two interactional pathological processes of atherosclerosis (AS). Up to now, there is no ideal drug for decreasing these pathological changes. Gua Lou Er Chen decoction (GED) has been used to treat AS for several years. However, if GED could treat AS through reducing PGs accumulation and inflammation remains unknown. PURPOSE: This study was designed to illustrate whether GED could attenuate AS by reducing chondroitin sulphate proteoglycan (CSPG) expressions and alleviating inflammation. METHODS: In vivo study, apolipoprotein E-deficient mice were fed a high-fat diet to induce AS. In vitro study, oxidised low-density lipoprotein (ox-LDL) and tumour necrosis factor (TNF)-α were used to induce proteoglycans accumulation and inflammation changes of vascular smooth muscle cells (VSMCs) and RAW264.7 macrophages. Oil Red O was used to stain mouse aortic lipid plaque. Haematoxylin eosin staining was used to assess the pathological changes of aortic valve and thoracic aorta. Specialised kits were used to identify blood lipids and sGAGs. Immunofluorescence and immunohistochemistry was used to identify aortic valve CSPG and versican. Western blotting, enzyme-linked immunosorbent assay and quantitative reverse transcription-polymerase chain reaction were used to measure versican, interleukin (IL)-6, TNF-α, and chondroitin sulphate (CS) synthetase expressions. CCK-8 was used to measure the cells proliferation. RESULTS: In vivo experiments revealed that GED significantly improved hyperlipidemia, lowered lipid plaque deposition in the aorta, and increased plaque stability of AS mice. In addition, further studies revealed that GED lowered the sGAGs, CSPG, and versican levels and down-regulated CS synthetase and inflammatory factor expressions. In vitro experiments revealed that GED decreased TNF-α expression in the RAW264.7 macrophage supernatant stimulated by ox-LDL; decreased versican, CS-related synthetase, and IL-6 expressions; reduced VSMC proliferation stimulated by ox-LDL; down-regulated sGAG and versican expressions of VSMCs stimulated by TNF-α. CONCLUSION: Our results demonstrated that GED could attenuate AS by reducing hyperlipidemia, hyper-expression of CSPG, and inflammation. This study might provide a novel insight into the development of innovative drug for AS.

Identification of Metabolic Syndrome-Related miRNA-mRNA Regulatory Networks and Key Genes Based on Bioinformatics Analysis.

Metabolic syndrome, which affects approximately one-quarter of the world's population, is a combination of multiple traits and is associated with high all-cause mortality, increased cancer risk, and other hazards. It has been shown that the epigenetic functions of miRNAs are closely related to metabolic syndrome, but epigenetic studies have not yet fully elucidated the regulatory network and key genes associated with metabolic syndrome. To perform data analysis and screening of potential differentially expressed target miRNAs, mRNAs and genes based on a bioinformatics approach using a metabolic syndrome mRNA and miRNA gene microarray, leading to further analysis and identification of metabolic syndrome-related miRNA-mRNA regulatory networks and key genes. The miRNA gene set (GSE98896) and mRNA gene set (GSE98895) of peripheral blood samples from patients with metabolic syndrome from the GEO database were screened, and set|logFC|> 1 and adjusted P < 0.05 were used to identify the differentially expressed miRNAs and mRNAs. Differentially expressed miRNA transcription factors were predicted using FunRich software and subjected to GO and KEGG enrichment analysis. Next, biological process enrichment analysis of differentially expressed mRNAs was performed with Metascape. Differentially expressed miRNAs and mRNAs were identified and visualized as miRNA-mRNA regulatory networks based on the complementary pairing principle. Data analysis of genome-wide metabolic syndrome-related mRNAs was performed using the gene set enrichment analysis (GSEA) database. Finally, further WGCNA of the set of genes most closely associated with metabolic syndrome was performed to validate the findings. A total of 217 differentially expressed mRNAs and 158 differentially expressed miRNAs were identified by screening the metabolic syndrome miRNA and mRNA gene sets, and these molecules mainly included transcription factors, such as SP1, SP4, and EGR1, that function in the IL-17 signalling pathway; cytokine-cytokine receptor interaction; proteoglycan syndecan-mediated signalling events; and the glypican pathway, which is involved in the inflammatory response and glucose and lipid metabolism. miR-34C-5P, which was identified by constructing a miRNA-mRNA regulatory network, could regulate DPYSL4 expression to influence insulin ß-cells, the inflammatory response and glucose oxidative catabolism. Based on GSEA, metabolic syndrome is known to be closely related to oxidative phosphorylation, DNA repair, neuronal damage, and glycolysis. Finally, RStudio and DAVID were used to perform WGCNA of the gene sets most closely associated with metabolic syndrome, and the results further validated the conclusions. Metabolic syndrome is a common metabolic disease worldwide, and its mechanism of action is closely related to the inflammatory response, glycolipid metabolism, and impaired mitochondrial function. miR-34C-5P can regulate DPYSL4 expression and can be a potential research target. In addition, UQCRQ and NDUFA8 are core genes of oxidative phosphorylation and have also been identified as potential targets for the future treatment of metabolic syndrome.

Appetite Suppression and Interleukin 17 Receptor Signaling Activation of Colonic Mycobiota Dysbiosis Induced by High Temperature and High Humidity Conditions.

It is known that the microbiome affects human physiology, emotion, disease, growth, and development. Most humans exhibit reduced appetites under high temperature and high humidity (HTHH) conditions, and HTHH environments favor fungal growth. Therefore, we hypothesized that the colonic mycobiota may affect the host's appetite under HTHH conditions. Changes in humidity are also associated with autoimmune diseases. In the current study mice were fed in an HTHH environment (32°C ± 2°C, relative humidity 95%) maintained via an artificial climate box for 8 hours per day for 21 days. Food intake, the colonic fungal microbiome, the feces metabolome, and appetite regulators were monitored. Components of the interleukin 17 pathway were also examined. In the experimental groups food intake and body weight were reduced, and the colonic mycobiota and fecal metabolome were substantially altered compared to control groups maintained at 25°C ± 2°C and relative humidity 65%. The appetite-related proteins LEPT and POMC were upregulated in the hypothalamus (p < 0.05), and NYP gene expression was downregulated (p < 0.05). The expression levels of PYY and O-linked ß-N-acetylglucosamine were altered in colonic tissues (p < 0.05), and interleukin 17 expression was upregulated in the colon. There was a strong correlation between colonic fungus and sugar metabolism. In fimo some metabolites of cholesterol, tromethamine, and cadaverine were significantly increased. There was significant elevation of the characteristic fungi Solicoccozyma aeria, and associated appetite suppression and interleukin 17 receptor signaling activation in some susceptible hosts, and disturbance of gut bacteria and fungi. The results indicate that the gut mycobiota plays an important role in the hypothalamus endocrine system with respect to appetite regulation via the gut-brain axis, and also plays an indispensable role in the stability of the gut microbiome and immunity. The mechanisms involved in these associations require extensive further studies.

Use of autochthonous lactic acid bacteria starters to ferment mango juice for promoting its probiotic roles.

Strains of Leuconostoc mesenteroides, Pediococcus pentosaceus, and Lactobacillus brevis were identified from mango fruits by partial 16S rDNA gene sequence. Based on the ability of producing mannitol and diacetyl, Leuconostoc mesenteroides MPL18 and MPL39 were selected within the lactic acid bacteria isolates, and used as mixed starters to ferment mango juice (MJ). Both the autochthonous strains grew well in fermented mango juice (FMJ) and remained viable at 9.81 log cfu mL(-1) during 30 days of storage at 4°C. The content of total sugar of FMJ was lower than that of MJ, while the concentration of mannitol was higher than that of MJ, and the concentration of diacetyl was 3.29 ± 0.12 mg L(-1). Among detected organic acids including citric acid, gallic acid, lactic acid, and acetic acid, only citric acid and gallic acid were found in MJ, while all detected organic acids were found in FMJ. The concentration of lactic acid of FMJ was the highest (78.62 ± 13.66 mM) among all detected organic acids. The DPPH radical scavenging capacity of FMJ was higher than that of MJ. Total phenolic compounds were better preserved in FMJ. The acidity and sweetness had a noticeable impact on the overall acceptance of the treated sample.