Dimethyl Sulfoxide Group Research Articles

Nephroprotective role of resveratrol in renal ischemia-reperfusion injury: a preclinical study in Sprague-Dawley rats.

Renal ischemia-reperfusion injury (IRI) is a significant contributor to renal dysfunction, acute kidney injury (AKI), and associated morbidity and mortality. Resveratrol, a polyphenol and phytoalexin, is known for its anti-inflammatory, antioxidant, and anti-cancer properties. This study investigates the nephroprotective potential of resveratrol in a rat model of renal IRI. Twenty-eight male Sprague-Dawley rats were divided into four groups: Sham, IRI, DMSO, and Resveratrol. The Sham group underwent identical procedures without renal pedicle clamping, while the IRI group experienced 30min of ischemia followed by 2h of reperfusion. The DMSO group received dimethyl sulfoxide (DMSO) intraperitoneally 30min before ischemia, and the Resveratrol group received 30mg/kg resveratrol intraperitoneally 30min before ischemia. Biochemical parameters (Urea, creatinine, IL-1β, NF-κβ, SOD, GSH, Bcl-2, and caspase-3) and histopathological changes were assessed. IRI caused a substantial increase in serum creatinine, Urea, IL-1β, NF-κβ, and caspase-3 levels, while simultaneously decreasing SOD, GSH, and Bcl-2 levels. Resveratrol treatment mitigated these effects by lowering inflammatory and apoptotic markers, enhancing antioxidant defenses, and improving histological outcomes. Resveratrol demonstrates significant nephroprotective effects in renal IRI, primarily through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Investigation of the efficacy of different cryoprotectants in the freezing of testicular tissue and epididymal sperm: Spermatological parameters, tissue viability and PARP-1 gene expression

The presented study covers testicular tissue and epididymal spermatozoa cryopreservation processes in bulls and aims to investigate the effects of these applications on spermatological parameters, cell viability in testicular tissue, and the expression of the PARP-1 gene, a DNA repair enzyme. Testes of 20 bulls over 2 years old, slaughtered in a slaughterhouse, were used in the study. After spermatological evaluations, the semen obtained from the cauda epididymis was frozen in liquid nitrogen vapor according to the straw method and stored in liquid nitrogen (−196 °C). Testicular tissue pieces obtained from the testicles were frozen by the slow freezing method in cryotubes in diluents containing Dimethylsulfoxide (DMSO) and Ethylene Glycol (EG) cryoprotectants and stored in liquid nitrogen (−196 °C). The total motility (TM) (85.89 ± 12.83 %), progressive motility (PM) (54.02 ± 15.77 %), and kinematic parameter values of fresh sperm were significantly higher compared to the TM (57.62 ± 13.13 %), PM (29.60 ± 10.76 %), and kinematic parameter values after thawing (P < 0.05). Significant decreases in plasma membrane integrity (PMI) and viability and an increase in chromatin condensation and morphological disorders in the head, middle part, and tail regions were observed in post-thaw semen samples (P < 0.05). When the effects of DMSO and EG on cell viability after thaw in frozen testicular tissue were evaluated, it was observed that the cell viability values of testicular tissues frozen with EG (45.70 ± 10.00) were statistically significantly lower than those frozen with DMSO (51.20 ± 7.70) (P < 0.05). When the effects of both cryoprotectants on gene expression in tissue and semen samples were examined, it was determined that gene expression increased on average 0.19 ± 0.27 times in the tissue samples in the DMSO group compared to fresh tissue samples and 0.17 ± 0.19 times in the tissue samples in the EG group. It was determined that gene expression levels increased by an average of 1.20 ± 1.08 times in post-thaw epididymal spermatozoa samples compared to fresh semen samples. The results show that cryopreservation can activate cellular repair mechanisms by stimulating PARP-1 gene expression and affect gene expression by activating specific pathways in tissues and cells.

Globular Antifreeze Protein-Inspired Nanoparticle-Based Large-Scale T-Cell Cryoprotection System for Lymphoma Immunotherapy.

Large-scale biosafe T-cell cryopreservation is required to bring T-cell therapies to the market, but it remains challenging due to the cytotoxicity of common cryoprotectants [e.g., dimethyl sulfoxide (DMSO)] and unavoidable ice injuries to cells. Herein, inspired by natural globular antifreeze proteins, we establish a biocompatible zwitterionic magnetic nanoparticle (ZMNP)-based cryoprotection system, achieving large-scale cryopreservation of T cells for lymphoma immunotherapy. ZMNPs could form a globular hydration shell to inhibit water molecule aggregation as well as ice growth, and the surficial hydration strength-antifreeze performance relationship of ZMNPs was investigated. During the thawing process, ZMNPs possessed a magnetic field-mediated nanowarming property that enabled rapid heating and also facilitated easy magnetic separation for cell recovery. These combined effects resulted in a high post-thaw viability (>80%) of large-scale T-cell cryopreservation (20 mL). Notably, post-thaw T cells exhibited similar transcript profiles to fresh cells, while up- or downregulation of 1050 genes was found in the DMSO group. In a mouse E.G7-OVA lymphoma model, ZMNP-system-cryopreserved T cells achieved a tumor suppression rate of 77.5%, twice as high as the DMSO group. This work holds great promise for the application of advanced cryopreservation techniques in the development of therapeutic cellular products.

Effects of Ionizing Radiation on Intestinal Bile Acid Metabolism: Mechanism of the Radioprotective Effect of Glycoursodeoxycholic Acid

Radioactive intestinal injury is a common complication during radiotherapy of tumors. The aim of this study is to observe the effect of ionizing radiation on short-term changes in intestinal bile acids and to investigate the radioprotective effect of bile acids on intestinal cells. A rat model of small intestinal injury was constructed by exposing the abdomen of the rats to daily irradiation at 2 Gy for 4 d in succession. The bile acids were quantified using metabolomics analysis. IEC-6 cells, a small intestinal epithelial cell line, were divided into a dimethyl sulfoxide (DMSO) control group receiving DMSO and 0 Gy irradiation, a glycoursodeoxycholic acid (GUDCA) experimental group receiving GUDCA and 0 Gy irradiation, a DMSO irradiation group receiving DMSO and 10 Gy irradiation, and a GUDCA irradiation group receiving GUDCA and 10 Gy irradiation. Cell viability and cytotoxicity was assessed by CCK-8 assay test. The apoptosis rate of cells was determined by flow cytometry. The colony formation rate and the radiosensitivity of the cells were determined by colony formation assay on solid media. The expression levels of proteins associated with cell death were determined using Western blot. After exposure to irradiation, the small intestine tissues of the rats showed typical radioactive intestinal injury. In addition, various bile acids showed fluctuation before and after irradiation. Among the bile acids, GUDCA increased significantly at 3 d after irradiation, but returned to the pre-irradiation level at 7 d after irradiation. Compared with the control group, after GUDCA treatment at 20 μmol/L for 24 h, the cell viability rate after irradiation was significantly higher than that of the DMSO group (P<0.05); the expression levels of the proteins, including PARP, caspase-3, RIP, and GSDMD, were significantly lower than those in the control group (P<0.05). After GUDCA treatment at 20 μmol/L for 24 h and 48 h, the cell apoptosis rate of the cells after irradiation was lower than that of the DMSO group (P<0.05). Compared with the DMSO control group, the colony formation ability of the GUDCA experimental group was stronger than that of the DMSO group after irradiation at 0, 2, 4, and 6 Gy (P<0.05). D0, or the mean lethal dose, of the GUDCA group was 6.374, while that of the DMSO group was 4.572. Compared with the DMSO control group, the D0 value of the GUDCA treatment group increased, and the sensitization enhancement ratio (SER) was 0.717. After exposing the abdomen of rats to irradiation, the intestinal bile acid metabolism of the rats will change significantly, and GUDCA can produce radioprotective effects on intestinal cells to a certain extent.

The characteristics of frozen-thawed rooster sperm using various intracellular cryoprotectants

Cryopreservation of rooster semen is essential for conserving genetic resources, genetic improvement, and increasing productivity. However, the nature of avian sperm presents a global issue in ensuring superior frozen semen for artificial insemination. Thus, the present study aimed to evaluate the impact of using dimethylacetamide (DMA), dimethyl sulfoxide (DMSO), and ethylene glycol (EG) as cryoprotectants on post-thawed sperm motility, quality, antioxidant indicators, and fertilizing capacity. Twice a week, fresh semen ejaculates were collected from 15 adult roosters and immediately evaluated to constitute a pool from clean and qualified samples. The pooled semen was further diluted at a ratio of 1:2 (v/v) with an extender and then subjected to a freezing protocol in a liquid nitrogen vapor after adding a cryoprotectant solution containing 6% of either DMA, DMSO, or EG, respectively. After thawing, characteristics of sperm motion, quality, antioxidants, and fertilizing ability were evaluated and compared to fresh and cooled semen as controls. The results demonstrated that semen cooling negatively affected some parameters of sperm motility, quality, antioxidant biomarkers, and fertility. In comparison to the DMSO and EG groups, employing DMA considerably (P < 0.05) raised the percentages of sperm progressive motility, viability, plasma membrane intactness, and DNA integrity. The DMA group showed a significant increase in the catalase and glutathione reduced antioxidant enzyme activity and a reduction in nitric oxide and lipid peroxidation. After artificial insemination, the DMA and DMSO groups exhibited considerably (P < 0.05) better rates of hatchability and fertility than the EG group. It is concluded that freezing extenders containing 6% DMA is better than DMSO or EG to improve the post thaw semen quality and fertility in chickens.

Necrostatin-1 protects corneal epithelial cells by inhibiting the RIPK1/RIPK3/MLKL cascade in a benzalkonium chloride-induced model of necroptosis

PurposeBenzalkonium chloride (BAC) is commonly used as a preservative in ophthalmic medications, despite its potential to induce chemical injury. Extensive research has demonstrated that BAC can lead to adverse effects, including injuries to the ocular surface. Our study aimed to elucidate the underlying mechanism of necroptosis induced by BAC. MethodsHuman corneal epithelial (HCE) cells and mouse corneas were subjected to chemical injury, and the necrostatin-1 (Nec1) group was compared to the dimethylsulfoxide (DMSO) group. The extent of damage to HCE cells was assessed using CCK-8 and flow cytometry. Hematoxylin and eosin staining, as well as fluorescein sodium staining, were used to detect and characterize corneal injury. The activation of inflammatory cytokines and necroptosis-related proteins and genes was evaluated using Western blotting, immunofluorescence staining, and quantitative RT‒PCR. ResultsIn our study, the induction of necroptosis by a hypertonic solution was not observed. However, necroptosis was observed in HCE cells exposed to NaOH and BAC, which activated the receptor-interacting protein kinase 1 (RIPK1) - receptor-interacting protein kinase 3 (RIPK3) - mixed lineage kinase domain-like protein (MLKL) signaling pathway. In mouse corneal tissues, BAC could induce necroptosis and inflammation. The administration of Nec1 mitigated the inflammatory response and ocular surface damage caused by BAC-induced necroptosis in our experimental models. Furthermore, our in vivo experiments revealed that the severity of necroptosis was greater in the 3-day group than in the 7-day group. ConclusionsNecroptosis plays a role in the pathological development of ocular surface injury caused by exposure to BAC. Furthermore, our study demonstrated that the administration of Nec1 could mitigate the pathological effects of necroptosis induced by BAC in clinical settings.

Histone demethylase JMJD3 inhibits alveolar bone loss by regulating macrophage polarization in periodontitis

Objective: To investigate the expression of histone demethylase, Jumonji domain-containing protein 3 (JMJD3), in inflammatory periodontal tissues and its potential mechanism for the regulation of periodontitis. Methods: The results of single-cell sequencing of periodontal tissues published in the Gene Expression Omnibus (GEO) database in 2022 were analyzed. Nine gingival samples each from healthy and inflamed periodontal patients were collected during periodontal surgery or tooth extractions for immunohistochemical staining and real-time fluorescence quantitative PCR (RT-qPCR). Mice periodontitis models were constructed, and the experimental groups were: healthy control+saline group, silk ligation+saline group, silk ligation+GSK-J4(inhibitor of JMJD3) group. Lipopolysaccharide (LPS) derived from Porphyromonas gingivalis (Pg) (Pg-LPS) was used to mimic the periodontal inflammatory microenvironment. The macrophages were treated with small interfering RNA (siRNA) targeting Jmjd3 and the JMJD3 inhibitor GSK-J4. siRNA transfection experiments were grouped into the following: the NC group (negative control sequence transfection group), the siRNA-Jmjd3 group, the NC+LPS group, siRNA-Jmjd3+LPS group. Inhibitor experiments were grouped as dimethyl sulfoxide (DMSO) group, GSK-J4 group, DMSO+LPS group, GSK-J4+LPS group. Western blotting and immunofluorescence staining were used to explore the effects of JMJD3 on macrophage polarization and periodontal inflammation in the in vivo and in vitro settings. Results: RT-qPCR results showed that JMJD3 expression in gingival tissues of periodontitis patients (1.97±0.91) was significantly higher than that in healthy gingival tissues (1.00±0.33) (t=2.45, P=0.048). RT-qPCR results of in vitro experiments showed that either siRNA knockdown of JMJD3 or inhibition of JMJD3 using GSK-J4 promoted M1 polarization and inhibited M2 polarization in macrophages under inflammatory environment: the expression of arginase I (Arg 1) in the NC+LPS group (0.90±0.06) was significantly higher than that in the siRNA-Jmjd3+LPS group (0.61±0.11) (P<0.01); the expression of interleukin (Il)-6, Il-1β, and tumor necrosis factor alpha (Tnf-α) in the NC+LPS group (8.50±0.16, 5.56±0.20, 3.44±0.16) were significantly lower than those in the siRNA-Jmjd3+LPS group (14.63±0.48, 8.55±0.10, 11.72±0.16) (P<0.01). The expression of Arg-1, Ym1, Il-10 in the DMSO+LPS group (0.82±0.01, 0.35±0.16, 1.47±0.11) were significantly higher (P<0.01) than the GSK-J4+LPS group (0.55±0.03, 0.22±0.21, 0.51±0.11); the expression of Il-6, Il-1β, and Tnf-α in the DMSO+LPS group (2.03±0.13, 3.63±0.14, 4.06±0.03) were significantly lower than the GSK-J4+LPS group (2.69±0.16, 15.04±1.15, 4.36±0.10) (P<0.01). The results of the in vivo experiments revealed that inhibition of JMJD3 exacerbated bone loss in experimental periodontitis mice, increased macrophage M1 polarization, and decreased M2 polarization in inflamed periodontal tissues. The buccal cemento-enamel junction (CEJ)-alveolar bone crest (ABC), palatal CEJ-ABC, as well as the ratio of M1/M2 type macrophages were significantly lower in the silk ligation+saline group [(0.26±0.03), (0.24±0.01) mm, 0.35±0.10) than in the silk ligation+GSK-J4 group [(0.34±0.04), (0.30±0.05) mm, 2.50±0.58) (t=3.65, P=0.006; t=2.67, P=0.049; t=7.31, P=0.004; respectively). Conclusions: Single-cell sequencing as well as the in vitro and in vivo experiments verified that JMJD3 expression was upregulated in periodontitis periodontal tissues. JMJD3 may exert a protective role in periodontitis by regulating macrophage polarization, thereby inhibiting alveolar bone destruction associated with the periodontitis.

Role of heads and tails on tetrahydrofuran- and dimethyl sulfoxide-water separation by glycerol and sucrose esters

Tetrahydrofuran (THF) and dimethylsulfoxide (DMSO) are miscible in water due to hydrogen (H) bonding. Amphiphilic glycerol and sucrose esters with a different number of tails and heads separate them, depending on the organic solvent concentration. Separation is worse in solutions where amphiphiles are most soluble. Separation occurs due to interactions between the amphiphiles and either organic solvents or water, as shown by attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR). Separation is best with glycerol esters with more heads and tails. Multiple tails hamper interactions between glycerol ester heads, thereby facilitating interactions with organic solvents or water to promote solvent–water separation. THF interacts with the glycerol ester tails, while water H bonds with the glycerol ester heads, as indicated by activity coefficients estimated with conductor-like screening model for real solvents. In THF, amphiphiles self-assemble into micelles, as shown by small angle x ray scattering (SAXS). Without water, THF is likely both inside and outside the micelles. SAXS shows that micelles shrink with 4% water in THF because water molecules partition inside them and are smaller than THF. With additional water, micelles swell into emulsions. Dissimilar to THF, DMSO preferentially interacts with the glycerol ester heads rather than their tails. ATR-FTIR shows that the proportion of free vs bonded S=O groups of DMSO decreases upon mixing with glycerol esters. DMSO and glycerol esters primarily accept H bonds, as indicated by their sigma profile. This leads to competition for interactions with water, displacing DMSO.

Astaxanthin Expedites the Healing of Acute Skin Wounds in Rats by Facilitating M2 Macrophage Polarization and Enhancing Collagen Secretion.

Facilitating the healing process of skin post-trauma is crucial for minimizing infection risks and reinstating normal tissue functionality. While past studies have established astaxanthin (ASX) as an effective compound in promoting wound healing, the precise mechanism of its action remains unclear. Consequently, the objective of this study was to explore the impact of ASX on the acute wound healing of rat skin by modulating macrophage polarization. Eighteen male SD rats were randomly assigned to control, dimethylsulfoxide (DMSO), and ASX groups. Acute skin wounds were induced in the rats, and the effects of different treatments on wound area and healing were assessed. Hematoxylin-eosin (H&E) staining was employed to detect histopathological changes in the skin, while Masson staining was utilized to observe collagen expression. Immunohistochemistry was conducted to identify clusters of differentiation (CD) 206 macrophages in the tissues. Furthermore, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, IL-10, IL-4, and IL-13. The expression of inducible nitric oxide synthase (iNOS), arginase (Arg)-1, and mannose receptor C-type 1 (Mrc1) proteins in the injured skin of rats was assessed through Western blot analysis. On postoperative days 7 and 14, the ASX treatment demonstrated notable reductions in inflammatory cell infiltration and inflammatory cytokine expression when compared to the Control and DMSO groups. This was accompanied by evident improvements in the pathological changes in skin tissue, characterized by the regeneration of new epidermis, dermal repair, and increased thickness of granulation, contributing to enhanced scar formation. Furthermore, ASX therapy exhibited an upregulation in the expression levels of collagen I and collagen III, along with markers indicative of M2 macrophages. These findings collectively signify the accelerated progression of wound healing attributed to ASX intervention. In summary, these findings collectively indicate that ASX facilitates the healing of rat skin wounds by suppressing inflammatory responses and fostering M2 macrophage polarization. Consequently, ASX holds promise as a potentially effective drug for the treatment of skin wounds.

Breviscapine ameliorates autophagy by activating the JAK2/STAT5/BCL2 pathway in a transient cerebral ischemia rat model.

Breviscapine (Bre), an extract from Erigeron breviscapus, has been widely used to treat cerebral ischemia but the mechanisms of its neuroprotective effects need to be clarified. The present study investigated whether Bre could alleviate excessive autophagy induced by cerebral ischemia in the rat middle cerebral artery occlusion (MCAO) ischemia model via activating the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5)/B-cell lymphoma 2 (BCL2) pathway. Rats were randomly divided into 5 groups, i.e. Sham group, MCAO+saline group, MCAO+Bre group, MCAO+DMSO (Dimethyl sulfoxide) group, and MCAO+Bre+AG490 (Tyrphostin AG490, the inhibitor of STAT5) group. The model was established and neuroprotection was evaluated by determining infarct volumes and conducting neurological behavioral tests. Autophagy levels in the infarct penumbra were detected using transmission electron microscopy and Western blotting. The expression of proteins in the JAK2/STAT5/BCL2 pathway was tested by Western blotting. Compared to the MCAO+saline group, the infarct volumes in the MCAO+Bre group were significantly reduced and neurological behavior improved. Breviscapine administration also significantly increased p-JAK2, p-STAT5, and BCL2 expression but decreased autolysosome numbers; it also downregulated Beclin-1 expression and the LC3II/LCI ratio. The JAK2 inhibitor AG490 reversed these effects. These findings indicate that breviscapine can improve neural recovery following ischemia through alleviating excessive autophagy and activation of the JAK2/STAT5/BCL2 axis.

Central Carbon Metabolism in Candida albicans Biofilms Is Altered by Dimethyl Sulfoxide.

The effect of dimethyl sulfoxide (DMSO) on fungal metabolism has not been well studied. This study aimed to evaluate, by metabolomics, the impact of DMSO on the central carbon metabolism of Candida albicans. Biofilms of C. albicans SC5314 were grown on paper discs, using minimum mineral (MM) medium, in a dynamic continuous flow system. The two experimental conditions were control and 0.03% DMSO (v/v). After 72 h of incubation (37 °C), the biofilms were collected and the metabolites were extracted. The extracted metabolites were subjected to gas chromatography-mass spectrometry (GC/MS). The experiment was conducted using five replicates on three independent occasions. The GC/MS analysis identified 88 compounds. Among the 88 compounds, the levels of 27 compounds were markedly different between the two groups. The DMSO group exhibited enhanced levels of putrescine and glutathione and decreased levels of methionine and lysine. Additionally, the DMSO group exhibited alterations in 13 metabolic pathways involved in primary and secondary cellular metabolism. Among the 13 altered pathways, seven were downregulated and six were upregulated in the DMSO group. These results indicated a differential intracellular metabolic profile between the untreated and DMSO-treated biofilms. Hence, DMSO was demonstrated to affect the metabolic pathways of C. albicans. These results suggest that DMSO may influence the results of laboratory tests when it is used as a solvent. Hence, the use of DMSO as a solvent must be carefully considered in drug research, as the effect of the researched drugs may not be reliably translated into clinical practice.

Curcumin inhibits the proliferation and migration of osteosarcoma by regulating the expression of super-enhancer-associated genes.

Super-enhancer-associated genes may be closely related to the progression of osteosarcoma, curcumin exhibits a certain inhibitory effect on tumors such as osteosarcoma. This study aims to investigate the effects of curcumin on osteosarcoma in vitro and in vivo, and to determine whether curcumin can inhibit the progression of osteosarcoma by suppressing the expression of super-enhancer-associated genes LIM and senescent cell antigen-like-containing domain 1 (LIMS1), secreted protein acidic and rich in cysteine (SPARC), and sterile alpha motif domain containing 4A (SAMD4A). Human osteosarcoma cell lines (MG63 cells or U2OS cells) were treated with 5 to 50 μmol/L curcumin for 24, 48, and 72 hours, followed by the methyl thiazolyl tetrazolium (MTT) assay to detect cell viability. Cells were incubated with dimethyl sulfoxide (DMSO) or curcumin (2.5, 5.0 μmol/L) for 7 days, and a colony formation assay was used to measure in vitro cell proliferation. After treatment with DMSO or curcumin (10, 15 μmol/L), a scratch healing assay and a transwell migration assay were performed to evaluate cell migration ability. Real-time reverse transcription polymerase chain reaction (real-time RT-PCR) and Western blotting were used to detect mRNA and protein expression levels of LIMS1, SPARC, and SAMD4A in the cells. An osteosarcoma-bearing nude mouse model was established, and curcumin was administered via gavage for 14 days to assess the impact of curcumin on tumor volume and weight in vivo. Real-time RT-PCR was used to measure mRNA expression levels of LIMS1, SPARC, and SAMD4A in the cancer and adjacent tissues from 12 osteosarcoma patients. After treating cells with different concentrations of curcumin for 24, 48, and 72 hours, cell viability were all significantly decreased. Compared with the DMSO group, the colony formation rates in the 2.5 μmol/L and 5.0 μmol/L curcumin groups significantly declined (both P<0.01). The scratch healing assay showed that, compared with the DMSO group, the migration rates of cells in the 10 μmol/L and 15 μmol/L curcumin groups were significantly reduced. The exception was the 10 μmol/L curcumin group at 24 h, where the migration rate of U2OS cells did not show a statistically significant difference (P>0.05), while all other differences were statistically significant (P<0.01 or P<0.001). The transwell migration assay results showed that the number of migrating cells in the 10 μmol/L and 15 μmol/L curcumin groups was significantly lower than that in the DMSO group (both P<0.001). In the in vivo tumor-bearing mouse experiment, the curcumin group showed a reduction in tumor mass (P<0.01) and a significant reduction in tumor volume (P<0.001) compared with the control group. Compared with the DMSO group, the mRNA expression levels of LIMS1, SPARC, and SAMD4A in the 10 μmol/L and 15 μmol/L curcumin groups were significantly down-regulated (all P<0.05). Additionally, the protein expression level of LIMS1 in U2OS cells in the 10 μmol/L curcumin group was significantly lower than that in the DMSO group (P<0.05). Compared with adjacent tissues, the mRNA expression level of SPARC in osteosarcoma tissues was significantly increased (P<0.001), while the mRNA expression levels of LIMS1 and SAMD4A did not show statistically significant differences (both P>0.05). Curcumin inhibits the proliferation and migration of osteosarcoma both in vitro and in vivo, which may be associated with the inactivation of super-enhancer-associated gene LIMS1.

The role of curcumin during pregnancy on the exposed fetuses’ tissues of Wistar rats to electromagnetic field

ABSTRACT To investigate curcumin (CUR) as the protector against the harmful effects of low-frequency electromagnetic field(LF- EMF, 50 Hz) during pregnancy period, 5 males and 15 females of Wistar rat mated and vaginal plaques were observed. Then, the pregnant rats were divided into six groups. During pregnancy(21 days), the EMF group was exposed to EMF for 30 min/day, the CUR group received a single dose of 50 mg/kg/daily CUR intraperitoneal, the EMF+CUR group was injected CUR and exposed to EMF daily. The DMSO(dimethyl sulfoxide) group was injected solvent of CUR (DMSO) intraperitoneal with the same volume of CUR solvent, the sham group was placed through the solenoid in the same conditions as the first group without exposure and the control group was kept in their cage in normal condition. After four weeks, babies born were divided according to the mother groups and sacrificed. Then, the three tissues injuries were investigated. EMF exposure led to an increase in outstanding necrotic areas in hippocampal tissue, an increase in the amount of hyperemia(p = 0.017) and necrotic(p = 0.005) in kidneys, and degeneration in liver tissue(p = 0.007) in the EMF group compared with EMF+CUR groups. A single dose of CUR daily during pregnancy can protect these tissues from injuries caused by LF-EMF exposure in rat fetuses.

Exploring the staining potential of 1 GSK-3 inhibitors in bovine teeth: 2 a one-year laboratory investigation.

GSK-3 inhibitors, such as Tideglusib (TG) and CHIR-99021 (CHIR), show promise in stimulating reparative dentin formation. The aim of this study was to assess the discoloration potential of TG and CHIR in an established in vitro model. Enamel-dentin specimens made from bovine incisors were randomly allocated to five groups (n=15 each): group bovine blood (BB), group dimethyl sulfoxide (DMSO), group TG, group CHIR, and group mineral trioxide aggregate (MTA). Each specimen had a central cavity in which the respective material was applied and sealed with resin-based luting material. Color determination was conducted using a dental spectrophotometer at t0 (before filling), t1 (immediately after filling), t2 (after one week), t3 (after one month), t4 (after three months), t5 (after six months), and t6 (after one year). Statistical analysis involved descriptive statistics, Kruskal-Wallis tests, and analysis of variance (α=0.05). Group BB and group CHIR exhibited the most significant decrease in lightness (ΔL*) after one year (ΔL*-4.7 and ΔL* -5.7, respectively), whereas groups DMSO, TG, and MTA showed minimal changes (DMSO ΔL*: -0.3; TG ΔL*: 1.4; MTA ΔL*: -0.5). Group BB and CHIR exhibited the highest ΔE values (6.4Å}0.6 and 6.5Å}0.8, respectively). Unlike CHIR, TG did not result in discoloration exceeding the threshold of visual perception, defined by a ΔE value of 5.5, during the one-year observation period. This laboratory study therefore suggests that TG could be utilized for indirect or direct pulp capping without major discoloration concerns. However, additional research is required to corroborate these findings.

Effect of Different Chemical Solvents on Bond Strength of Orthodontic Brackets: An In Vitro Study.

The purpose of the present study was to evaluate the impact of various chemical solvents on bond strength of orthodontic brackets. One hundred healthy human premolars with undamaged buccal surfaces that were extracted for orthodontic purposes were gathered. Using 37% orthophosphoric acid, primer, and Transbond XT adhesive, ceramic 0.018" × 0.022" slot orthodontic brackets were adhered to the tooth surface. Following thermocycling, all samples were divided into four groups, with 25 samples in each group: group I: control; group II: application of ethanol; group III: application of acetone; and group IV: application of dimethyl sulfoxide (DMSO). Following the debonding tests, a double-ocular stereomicroscope was used to inspect the tooth surfaces. Additionally, adhesive remnant index (ARI) values were evaluated at 40× magnification. Data were recorded and statistically analyzed. The bond strength was lesser in acetone applied group (16.18 ± 3.64) followed by DMSO applied group (22.08 ± 2.86), ethanol applied group (24.36 ± 4.02), and control group (27.14 ± 3.68). There was a highly significant difference found between the chemical solvents group. The ARI score 3 was present in control (12%), ethanol (8%), and DMSO (4%), and it was absent in acetone applied group. The ARI score 0 was more in acetone applied group (24%). The present study concluded that the reduced debonding force was found with the application of acetone solvent followed by DMSO, ethanol, and control groups. Applying acetone can be a substitute technique to help with ceramic bracket debonding. Orthodontic bracket debonding cannot occur without shear bond strength (SBS). The need for an ideal debonding technique for ceramic brackets without negative consequences arises from the risk of enamel damage that frequently follows the process. Acetone treatment prior to ceramic bracket debonding could be an alternate clinical technique to preventing enamel damage and facilitating debonding. How to cite this article: Bhushan R, Singh S, Sam G, et al. Effect of Different Chemical Solvents on Bond Strength of Orthodontic Brackets: An In Vitro Study. J Contemp Dent Pract 2023;24(12):940-943.

Effect of Prepartum Maternal Supplementation with Diphenyl Diselenide on Biochemical, Immunological, and Oxidative Parameters of the Offspring.

This study aimed to assess the impact of prepartum maternal diphenyl diselenide (PhSe)2 supplementation on the development, biochemical, immune, and antioxidant parameters of calves. Eighteen Holstein breed calves were used, born to females who were or were not subjected to supplementation, at 42, 28, and 14 days prior to calving. The (PhSe)2 group (DDG) was administered 3 μmol/kg of (PhSe)2 in 4 mL of dimethyl sulfoxide (DMSO), while the DMSO and NaCl groups were administered 4 mL of DMSO and 0.9% NaCl, subcutaneously. The calves were evaluated based on their weight, withers height, body condition score 24 h post-birth (0), as well on days 14, 28, 42, 56, 70. Blood samples were also taken to determine serum variables. Calves on the DDG showed higher average levels of total protein, albumin, and globulins on day 0, and the immunoglobulin G level was significantly higher than the other groups on days 0, 14, 56, 70. Maternal supplementation showed immunomodulatory effect on calves, evidenced by the exceptional rates of passive immunity transfer, as well as the enhancement of humoral immunity. Our research offers fresh insights into the immunomodulatory potential of (PhSe)2, making it a viable alternative in facing this challenging phase, rearing dairy calves.

Uroprotective effects of berberine and curcumin in cyclophosphamide-induced interstitial cystitis.

In this study, it was aimed to investigate the effects of berberine (BER) and curcumin (CUR) in the experimental model of cystitis induced by cyclophosphamide (CYP). A total of 36 Wistar-Albino female rats were used in the study. Rats were randomly divided into six groups (n = 6). Normal control group, dimethyl sulfoxide (DMSO) group, CYP group (75 mg/kg), CYP + BER (75 mg/kg CYP and 50 mg/kg BER), CYP + CUR group (75 mg/kg CYP and 50 mg/kg CUR), CYP + BER + CUR group (75 mg/kg CYP and 50 mg/kg BER and 50 mg/kg CUR). Severe edema, hyperemia, hemorrhage, necrosis, and thinning of the epithelial layer were observed in the CYP group. BER and CUR treatment significantly reduced these pathologies. Masson-Trichrome staining was severe in the CYP group and moderate in the CYP + BER, CYP + CUR, and CYP + BER + CUR groups. In the CYP group, there was a severe expression of caspase-3, TNF-α and IL-6, and mild expression of IL-10. BER and CUR treatment decreased the expression of caspase-3, TNF-α, and IL-6 and increased the expression of IL-10. The findings of the study reveal that BER and CUR treatments may reduce CYP-induced bladder damage by reducing apoptosis and inflammation and ameliorating histopathological changes.

Experimental study on the therapeutic effect and mechanism of erlotinib on non-proliferative diabetic retinopathy

Experimental study on the therapeutic effect and mechanism of erlotinib on non-proliferative diabetic retinopathy

Effect of AT1 receptor blockade on cardiovascular outcome after cardiac arrest: an experimental study in rats

Angiotensin II receptor 1(AT1) antagonists are beneficial in focal ischemia/reperfusion (I/R). However, in cases of global I/R, such as cardiac arrest (CA), AT1 blocker's potential benefits are still unknown. Wistar male rats were allocated into four groups: Control group (CG)—animals submitted to CA by ventricular fibrillation induced by direct electrical stimulation for 3 min, and anoxia for 5 min; Group AT1 (GAT1)—animals subjected to CA and treated with 0.2 mg/kg of candesartan diluted in dimethylsulfoxide (DMSO) (0.1%); Vehicle Group (VG): animals subjected to CA and treated with 0.2 ml/kg of DMSO and Sham group (SG)—animals submitted to surgical interventions, without CA. Cardiopulmonary resuscitation consisted of group medications, chest compressions, ventilation, epinephrine (20 mcg/kg) and defibrillation. The animals were observed up to 4 h after spontaneous circulation (ROSC) return, and survival rates, hemodynamic variables, histopathology, and markers of tissue injury were analyzed. GAT1 group had a higher rate of ROSC (62.5% vs. 42.1%, p < 0.0001), survival (100% vs. 62.5%, p = 0.027), lower incidence of arrhythmia after 10 min of ROSC (10% vs. 62.5%, p = 0.000), and lower neuronal and cardiac injury scores on histology evaluation (p = 0.025 and p = 0.0052, respectively) than GC group. The groups did not differ regarding CA duration, number of adrenaline doses, or number of defibrillations. AT1 receptor blockade with candesartan yielded higher rates of ROSC and survival, in addition to neuronal and myocardial protection.

Synergistic Effects of Capsaicin and Quercetin Improved Induced Premature Ovarian Failure in Rat.

Premature ovarian failure (POF) is a heterogeneous disorder. POF is defined as hypergonadotropic hypoestrogenism in women under 40 years. There is no effective treatment to cure POF patients. Antioxidants prevent ovarian damage by reducing the lipid peroxidation cascades affecting folliculogenesis, meiosis and ovulation. Hence; the aim of present study was to investigate the effects of Capsaicin (CAP) and Quercetin (QUR) on cyclophosphamide (CYC)-induced POF in rat model. In this experimental study, POF was induced by intraperitoneal injection of 200 mg/kg CYC on first day and then 8 mg/kg/day for the following 3 days. After 4 days of CYC administration, rats were randomly divided into five groups (n=6/group) as follows: POF, dimethyl sulfoxide (DMSO), CAP (0.5 mg/kg/day), QUR (100 mg/kg/day) and CAP+QUR. Biochemical, hormonal, gene expression, and histological evaluations were performed on blood serum and tissue samples after 14 days of treatment with the CAP and QUR. CAP, QUR and CAP+QUR groups showed signs of restored ovarian function in the form of a significant increase in serum total antioxidant capacity (TAC), estrogen, progesterone and anti-mullerian hormone (AMH) levels versus POF and DMSO groups and a significant improvement in histological parameters and follicle numbers in treatment groups compared to POF and DMSO groups. Polymerase chain reaction (PCR) analysis demonstrated that CAP and QUR upregulate the expression of BAX gene and decreased the expression of apoptosis inducing genes (BCL-2 and P53). CAP and QUR treatment of CYC-induced POF rats showed a positive effect on reducing ovarian damage by improving TAC levels, expression of apoptotic genes, levels of ovarian reserve markers, and histological parameters. Our results suggest that treatment with CAP or QUR may be a conservative treatment approach for CYC -induced POF.