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Autoimmune diseases (AID) have emerged as prominent contributors to disability and mortality worldwide, characterized by intricate pathogenic mechanisms involving genetic, environmental, and autoimmune factors. In response to this challenge, a growing body of research in recent years has delved into genetic modifications, yielding valuable insights into AID prevention and treatment. Sirtuins (SIRTs) constitute a class of NAD-dependent histone deacetylases that orchestrate deacetylation processes, wielding significant regulatory influence over cellular metabolism, oxidative stress, immune response, apoptosis, and aging through epigenetic modifications. Resveratrol, the pioneering activator of the SIRTs family, and its derivatives have captured global scholarly interest. In the context of AID, these compounds hold promise for therapeutic intervention by modulating the SIRTs pathway, impacting immune cell functionality, suppressing the release of inflammatory mediators, and mitigating tissue damage. This review endeavors to explore the potential of resveratrol and its derivatives in AID treatment, elucidating their mechanisms of action and providing a comprehensive analysis of current research advancements and obstacles. Through a thorough examination of existing literature, our objective is to advocate for the utilization of resveratrol and its derivatives in AID treatment while offering crucial insights for the formulation of innovative therapeutic approaches.

Sirtuins (SIRTs) represent a class of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases that exert a crucial role in cellular signal transduction and various biological processes. The mammalian sirtuins family encompasses SIRT1 to SIRT7, exhibiting therapeutic potential in counteracting cellular aging, modulating metabolism, responding to oxidative stress, inhibiting tumors, and improving cellular microenvironment. These enzymes are intricately linked to the occurrence and treatment of diverse pathological conditions, including cancer, autoimmune diseases, and cardiovascular disorders. Given the significance of histone modification in gene expression and chromatin structure, maintaining the equilibrium of the sirtuins family is imperative for disease prevention and health restoration. Mounting evidence suggests that modulators of SIRTs play a crucial role in treating various diseases and maintaining physiological balance. This review delves into the molecular structure and regulatory functions of the sirtuins family, reviews the classification and historical evolution of SIRTs modulators, offers a systematic overview of existing SIRTs modulation strategies, and elucidates the regulatory mechanisms of SIRTs modulators (agonists and inhibitors) and their clinical applications. The article concludes by summarizing the challenges encountered in SIRTs modulator research and offering insights into future research directions.

Abstract Binderless particleboards were prepared without any resin adhesives from Broussonetia papyrifera trunk by hot pressing. The effects of particle size, pressing time, pressing temperature and board density on the physical and mechanical properties of binderless boards were investigated. The effects of chemical changes in Broussonetia papyrifera binderless particleboards on the board properties were investigated by chemical, spectroscopic and cellulose crystallinity analyses. The bonding performance of the latex of Broussonetia papyrifera was discussed. The results showed: (1) the smaller size of the particle, the higher internal bonding (IB) strength and lower thickness swelling (TS) of the binderless board had. The modulus of rupture (MOR), the modulus of elasticity (MOE) and the IB values of the boards increased with the increase of board density. Within a certain range, the binderless boards manufactured at higher temperature and longer pressing time had better properties. Under the optimum board manufacturing condition of 220 ℃/30 min/1.0 g/cm3, the Broussonetia papyrifera binderless board recorded a MOR 28 MPa, MOE 5.3 GPa, IB 2.74 MPa and 24 h TS of 7.4%, which met the performance requirements of Chinese national standard for heavy-duty particleboard. (2) The degradation of cellulose and hemicellulose during hot pressing resulted in decrease of cellulose and hemicellulose content and increase of extractives. Some of the degradation products form new bonding to increase the bonding strength and dimensional stability of the binderless boards. (3) The formation of pseudo-lignin and increased C–O–C and cellulose crystallinity of the boards during hot pressing contributed to high quality of the binderless boards. (4) The poplar veneers bonded with the latex of Broussonetia papyrifera had a certain bonding strength (0.6 MPa), indicating the latex played a positive role in self-bonding of the Broussonetia papyrifera particleboard.

In recent years, epigenetic modifications have been widely researched. As humans age, environmental and genetic factors may drive inflammation and immune responses by influencing the epigenome, which can lead to abnormal autoimmune responses in the body. Currently, an increasing number of studies have emphasized the important role of epigenetic modification in the progression of autoimmune diseases. Sirtuins (SIRTs) are class III nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylases and SIRT-mediated deacetylation is an important epigenetic alteration. The SIRT family comprises seven protein members (namely, SIRT1–7). While the catalytic core domain contains amino acid residues that have remained stable throughout the entire evolutionary process, the N- and C-terminal regions are structurally divergent and contribute to differences in subcellular localization, enzymatic activity and substrate specificity. SIRT1 and SIRT2 are localized in the nucleus and cytoplasm. SIRT3, SIRT4, and SIRT5 are mitochondrial, and SIRT6 and SIRT7 are predominantly found in the nucleus. SIRTs are key regulators of various physiological processes such as cellular differentiation, apoptosis, metabolism, ageing, immune response, oxidative stress, and mitochondrial function. We discuss the association between SIRTs and common autoimmune diseases to facilitate the development of more effective therapeutic strategies.

Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by destruction of synovial joints, abnormal immune responses and chronic inflammatory manifestations, which seriously affects patients’ well-being. We explored this study to ascertain the effect and mechanism of silent information regulator 6 (SIRT6) on RA. Methods: Genes of RA patients and normal volunteers were analyzed using Gene Expression Omnibus (GEO), Kyoto-Encyclopedia of Genes and Genomes (KEGG) and Disconet databases. Serum samples of RA patients and normal subjects were collected before detection of myeloid differentiation factor-88 (MyD88)-extracellular signal-regulated kinase (ERK) pathway proteins expression with Western blot. In vitro RA fibroblast-like synoviocytes (FLS) cell model (RA-FLS) was established by treating RSC-364 with recombinant rat IL-1β (10 ng/mL) after which SIRT6 and MyD88 adenoviruses treatment was carried out. The enzyme linked immunoassay (ELISA), real time polymerase chain reaction (RT-PCR) and Western blot were respectively used to measure inflammatory factors, related messenger ribonucleic acid (mRNA) and protein expressions. Also, we constructed RA rat model with bovine type II collagen (BIIC) and complete Freund’s adjuvant, before treatment with SIRT6 and MyD88 adenoviruses. Results: Low expression of SIRT6 gene were detected in RA patients. Also, levels of MyD88, ERK and phosphorylated extracellular signal-regulated protein kinase (p-ERK) protein expressions in RA patients were increased, whilst that of SIRT6 protein decreased. Compared to FLS cells in Control group, inflammatory factors levels of rats in Model batch increased significantly. SIRT6 adenovirus treatment potentially and significantly inhibited inflammation including suppression of increased inflammatory factors induced by MyD88. In comparison with FLS cells in Control group, Model batch cells’ MyD88, interleukin (IL)-1β, IL-21, IL-22, IL-6, IL-17, tumor necrosis factor-alpha (TNF-α) and monocyte chemo-attractant protein-1 (MCP-1) mRNA expressions increased but SIRT6 gene treatment could reduce mRNA expression of the aforesaid factors, even after MyD88 adenovirus treatment. Besides, overpressed SIRT6 negatively regulated levels of MyD88, ERK and p-ERK proteins expressions. SIRT6 demonstrated anti-RA effect by regulating MyD88-ERK pathway and inhibiting inflammatory response in RA rats. Conclusions: SIRT6 could potentially inhibit the inflammatory response of RA via a regulatory mechanism mainly relating to MyD88-ERK signal pathway. Thus, SIRT6 and its agonists may serve as new targets for developing drugs that can potentially treat RA.

This study aimed to enhance the properties and interfacial compatibility of poplar veneer/polyethylene (PE) film composite plywood using heat treatment by prolonging the hot-pressing time. The plywood was heat-treated (long time hot-pressed) at 160, 180, and 200 °C for 2 h. The results showed that after being heat-treated at 180 °C for 2 h, the shear strength of the plywood was effectively increased from 0.49 MPa to 0.94 MPa, which met the requirements of type I plywood according to the Chinese National Standard GB/T 9846–2015. The higher the treatment temperature, the better the water resistance and durability of the plywood. The Fourier transform infrared spectroscopy (FTIR) spectra indicated that the number of hydroxyl groups and carbonyl groups was reduced after heat treatment, thus decreasing the surface hydrophilicity of poplar veneer. The scanning electron microscopy (SEM) images showed that heat-treated plywood possessed more continuous and uniform glueline compared with untreated plywood.

Considered as an autoimmune disease, rheumatoid arthritis (RA) is an chronic inflammatory disorder that causes inflammation of the joints. This study is performed with the aim to clarify the expression of phospholipase D1 (PLD1) in RA and its specific regulation role of RA as well as the underlying mechanisms. In this study, synovial tissue samples were collected from RA patients, and RA-fibroblast-like synoviocytes (FLSs) were subsequently isolated. The expression levels of PLD1 and pathway-related proteins were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting or immunohistochemistry (IHC). Upon shPLD1 treatment, cell viability, proliferation, migration, invasion, and the level of inflammation-related factors were measured by Cell Counting Kit-8 (CCK-8), Edu, wound healing, Transwell and enzyme-linked immunosorbent assay (ELISA). Furthermore, C-reactive protein (CRP), rheumatoid factor (RF), arthritis score and synovial tissue lesions were assessed by collecting the blood or tissues from collagen induced arthritis (CIA) model rats. Our results showed that PLD1 level was increased in RA synovial tissues. Cell viability, proliferation, migration, invasion, and the level of inflammatory factors were reduced upon PLD1 knockdown in RA-FLSs. Moreover, p-IκBα/IκBα, β-catenin, p-IKKβ/IKKβ and TCF-4 were inhibited under PLD1 knockdown treatment. PLD1 knockdown alleviated the collagen-induced addition of arthritis score, CRP and RF, as well as the filling of inflammatory cells and proliferation of synovium in CIA model rat. To sum up, knockdown of PLD1 could reduce RA-FLSs metastasis as well as inflammatory response by modulating the activity of NF-κB and Wnt/β-catenin pathways.

Abstract Chestnut bur is an agro-waste material generated in the chestnut production. It is a tannin-rich lignocellulosic material which might be a promising raw material for low-formaldehyde composite particleboard production when using urea–formaldehyde (UF) as bonding adhesive. In this study, the characteristics of chestnut bur were analyzed to assess its application value for composite panel. Five-type particleboards were manufactured from the mixture of chestnut bur/poplar particles with the weight ratios of 0/100, 25/75, 50/50, 75/25 and 100/0, UF resin was used as bonding adhesive. The effects of the addition amount of chestnut bur on the physical, mechanical properties and formaldehyde emission of particleboard were studied. The results showed as follows: (1) chestnut bur showed low cellulose, hemicelluloses and lignin contents, but high extractives and ash contents compared with poplar wood. Chestnut bur and poplar wood had the similar fiber morphology. (2) Composite board with relatively good performances could be manufactured with mix particles of chestnut bur and poplar wood. With the increasing of chestnut bur content, the mechanical properties of the composite board decreased, whereas the dimensional stability increased. (3) The total phenol content in the chestnut bur was as high as 13.79%. The phenolic substance in the chestnut burs could react with free formaldehyde. Hence, the free formaldehyde emission of particleboard was effectively reduced. In summary, waste chestnut bur is a suitable material which can not only be utilized as the base material, but also a natural free formaldehyde scavenger for composite particleboard production.