Sciadonic acid attenuates high-fat diet-induced bone metabolism disorders in mice.

High-fat diet (HFD) has been associated with certain negative bone-related outcomes, such as bone metabolism disruption and bone loss. Sciadonic acid (SC), one of the main nutritional and functional components of Torreya grandis seed oil, is a unique Δ5-unsaturated-polymethylene-interrupted fatty acid (Δ5-UPIFA) that has been claimed to counteract such disorders owing to some of its physiological effects. However, the role of SC in ameliorating bone metabolism disorders due to HFD remains unclear. In the present investigation, we observed that SC modulates the OPG/RANKL/RANK signaling pathway by modifying the lipid metabolic state and decreasing inflammation in mice. In turn, it could balance bone resorption and formation as well as calcium and phosphorus levels, enhance bone strength and bone mineral density (BMD), and improve its microstructure. In addition, SC could inhibit fat vacuoles in bone, reverse the phenomenon of reduced numbers and poor continuity of bone trabeculae, and promote orderly arrangement of collagen fibers and cartilage repair. This study provides some theoretical basis for SC as a dietary intervention agent to enhance bone nutrition.

Exploring the Regulatory Effect of Tegillarca granosa Polysaccharide on High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice Based on Intestinal Flora.

To explore the potential mechanism of action of Tegillarca granosa polysaccharide (TGP) in treating nonalcoholic fatty liver disease (NAFLD), the study conducts in vivo experiments using male C57BL/6 mice fed a high-fat diet while administering TGP for 16 weeks. The study measures body weight, liver weight, serum biochemical markers, pathological histology, liver lipid accumulation, oxidative stress and inflammation-related factors, lipid synthesis and metabolism-related gene and protein expression, and the composition and abundance of intestinal flora. Additionally, short-chain fatty acid (SCFAs) content and the correlation between intestinal flora and environmental factors are measured. The results show that TGP effectively reduces excessive hepatic lipid accumulation, dyslipidemia, abnormal liver function, and steatosis in the mice with NAFLD. Moreover, TGP effectively regulates intestinal flora disorder, increases the diversity of intestinal flora, and affects the relative abundance of specific bacteria while also increasing the content of SCFAs. These findings provide a basis for exploring the regulatory effect of T. granosa polysaccharide on NAFLD based on intestinal flora and highlight its potential as a natural liver nutraceutical.

Sciadonic acid ameliorates cyclophosphamide-induced immunosuppression by modulating the immune response and altering the gut microbiota.

BACKGROUND: Cyclophosphamide (Cy) is a frequently used chemotherapeutic drug, but long-term Cy treatment can cause immunosuppression and intestinal mucosal damage. The intestinal mucosal barrier and gut flora play important roles in regulating host metabolism, maintaining physiological functions and protecting immune homeostasis. Dysbiosis of the intestinal flora affects the development of the intestinal microenvironment, as well as the development of various external systemic diseases and metabolic syndrome. RESULTS: The present study investigated the influence of sciadonic acid (SA) on Cy-induced immunosuppression in mice. The results showed that SA gavage significantly alleviated Cy-induced immune damage by improving the immune system organ index, immune response and oxidative stress. Moreover, SA restored intestinal morphology, improved villus integrity and activated the nuclear factor κB signaling pathway, stimulated cytokine production, and reduced serum lipopolysaccharide (LPS) levels. Furthermore, gut microbiota analysis indicated that SA increased t beneficial bacteria (Alistipes, Lachnospiraceae_NK4A136_group, Rikenella and Odoribacter) and decreased pathogenic bacteria (norank-f-Oscillospiraceae, Ruminococcus and Desulfovibrio) to maintain intestinal homeostasis. CONCLUSION: The present study provided new insights into the SA regulation of intestinal flora to enhance immune responses. © 2024 Society of Chemical Industry.

Boesenbergia rotunda displayed anti-inflammatory, antioxidant and anti-apoptotic efficacy in doxorubicin-induced cardiotoxicity in rats.

This study evaluated the cardioprotective properties of Boesenbergia rotunda extract (BrE) against doxorubicin (DOX) induced cardiotoxicity. Rats received oral gavage of BrE for 28 days and DOX (5 mg/kg/week for 3 weeks). Thereafter the animals were sacrificed, blood and cardiac samples were collected for biochemical, histological and immunohistochemical analyses. The results indicated that BrE attenuated DOX triggered body and cardiac weight loss and prevented against cardiac injury by mitigating histopathological alterations in cardiac tissues as well as serum cardiac function enzymes. BrE significantly reduced serum levels of aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), troponin T (TnT) and creatine kinase-MB (CK-MB) in DOX-treated rats. Furthermore, BrE alleviated cardiotoxicity by reducing DOX instigated oxidative stress and potentiating the level of glutathione, as well as the activities superoxide dismutase and catalase in cardiac tissues. In addition, BrE significantly decreased the characteristic indices of DOX-induced cardiac inflammation and apoptosis. Immuno-histochemical analysis revealed that BrE decreased the stain intensity of p53 and myeloperoxidase (MPO) proteins compared to the DXB alone group. In conclusion, our results indicated that BrE modulated oxidative stress, inflammation and apoptosis to attenuate DOX-induced cardiac damage.

Sciadonic acid attenuates high-fat diet-induced obesity in mice with alterations in the gut microbiota.

Obesity has been reported to be associated with dysbiosis of gut microbiota. Sciadonic acid (SC) is one of the main functional components of Torreya grandis "Merrillii" seed oil. However, the effect of SC on high-fat diet (HFD)-induced obesity has not been elucidated. In this study, we evaluated the effects of SC on lipid metabolism and the gut flora in mice fed with a high-fat diet. The results revealed that SC activates the PPARα/SREBP-1C/FAS signaling pathway and reduces the levels of total cholesterol (TC), triacylglycerols (TG), and low-density lipoprotein cholesterol (LDL-C), but increases the level of high-density lipoprotein cholesterol (HDL-C) and inhibits weight gain. Among them, high-dose SC was the most effective; the TC, TG and LDL-C levels were reduced by 20.03%, 28.40% and 22.07%, respectively; the HDL-C level was increased by 8.55%. In addition, SC significantly increased glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels by 98.21% and 35.17%, respectively, decreased oxidative stress, and ameliorated the pathological damage to the liver caused by a high-fat diet. Furthermore, SC treatment altered the composition of the intestinal flora, promoting the relative abundance of beneficial bacteria such as Lactobacillus and Bifidobacterium, while simultaneously decreasing the relative abundance of potentially harmful bacteria such as Faecalibaculum, norank_f_Desulfovibrionaceae, and Romboutsia. Spearman's correlation analysis indicated that the gut microbiota was associated with SCFAs and biochemical indicators. In summary, our results suggested that SC can improve lipid metabolism disorders and regulate the gut microbial structure.

Effect of mussel polysaccharide on glucolipid metabolism and intestinal flora in type 2 diabetic mice.

BACKGROUND: Type 2 diabetes (T2D) mellitus is a major metabolic disease, and its incidence and lethality have increased significantly in recent years, making it a serious threat to human health. Among numerous previous studies, polysaccharides have been shown to alleviate the adverse effects of T2D, but there are still problems such as insufficient analysis and poor understanding of the mechanisms by which polysaccharides, especially those of marine origin, regulate T2D. METHODS: In this study, we used multiple allosteric approaches to further investigate the regulatory effects of mussel polysaccharides (MPs) on T2D and gut microbiota disorders in mice by identifying changes in genes, proteins, metabolites and target organs associated with glucolipid metabolism using an animal model of T2D fed with high-fat diets, and to explore the underlying molecular mechanisms. RESULTS: After MP intervention, serum levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and high-density lipoprotein cholesterol (HDL-C) were up-regulated, and blood glucose and lipid levels were effectively reduced in T2D mice. Activation of signaling molecules related to the upstream and downstream of the insulin PI3K/Akt signaling pathway reduced hepatic insulin resistance. The relative abundance of short-chain fatty acid (SCFA)-producing bacteria (including Akkermansia, Siraeum Eubacterium and Allobaculum) increased and harmful desulfurizing Vibrio decreased. In addition, the levels of SCFAs were increased. CONCLUSION: These results suggest that MP can increase SCFA levels by altering the abundance of intestinal flora, thereby activating the PI3K/Akt signaling pathway and exerting hypoglycemic effects. © 2023 Society of Chemical Industry.

A review on shellfish polysaccharides: Extraction, characterization and amelioration of metabolic syndrome.

Shellfish are diverse, widely distributed organisms that are a rich source of biological resources. Polysaccharides are an important components in shellfish, hence a great deal of attention has been directed at isolation and characterization of shellfish polysaccharides because of their numerous health benefits. Differences in shellfish species, habits, and environment result in the diversity of the structure and composition of polysaccharides. Thus, shellfish polysaccharides possess special biological activities. Studies have shown that shellfish polysaccharides exert biological activities, including antioxidant, antitumor, immune-regulation, hypolipidemic, antihypertensive, and antihyperglycemic effects, and are widely used in cosmetics, health products, and medicine. This review spotlights the extraction and purification methods of shellfish polysaccharides and analyses their structures, biological activities and conformational relationships; discusses the regulatory mechanism of shellfish polysaccharides on hyperlipidemia, hypertension, and hyperglycemia caused by lipid metabolism disorders; and summarizes its alleviation of lipid metabolism-related diseases. This review provides a reference for the in-depth development and utilization of shellfish polysaccharides as a functional food to regulate lipid metabolism-related diseases. To achieve high value utilization of marine shellfish resources while actively promoting the development of marine biological industry and health industry.

Protective Effect of Oyster Peptides Derived From Crassostrea gigas on Intestinal Oxidative Damage Induced by Cyclophosphamide in Mice Mediated Through Nrf2-Keap1 Signaling Pathway.

Oyster peptide (OP) has exhibited useful biological activities and can be used in multi-functional foods. OP has been reported to play a significant role in intestinal protection, but its specific mechanism is still not completely understood. The aim of this study was to analyze the potential effect of OP on oxidative damage of mice intestine induced by cyclophosphamide (Cy). The experimental results revealed that intragastric administration of OP significantly increased average bodyweight, improved ileum tissue morphology and villus structure, as well as increased the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in oxidized mice serum and liver. The content of malondialdehyde (MDA) in the mice serum and liver homogenate was found to be markedly decreased. Moreover, OP significantly increased the relative mRNA expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), quinone oxidoreductase (NQO1) and heme oxidase-1 (HO-1) in ileum. Western-blot results indicated that prior administration of OP significantly up-regulated the Nrf2 production in ileum, and substantially decreased then Keap1 gene expression. In conclusion, intake of OP was found to markedly improve intestinal oxidative stress in vivo, and this effect was primarily mediated through the simulation of antioxidant Nrf2-Keap1 signaling pathway. This study is beneficial to the application of peptide nutrients in the prevention or mitigation of intestinal oxidative damage.

Antidiabetic effect of sciadonic acid on type 2 diabetic mice through activating the PI3K-AKT signaling pathway and altering intestinal flora.

Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by hyperglycemia. The aim of this work was to investigate the effect of sciadonic acid (SA) on disorders of glucolipid metabolism and intestinal flora imbalance and to further investigate its potential molecular mechanism of anti-diabetes. The experimental data indicated that SA could alleviate hyperlipidemia, insulin resistance, oxidative stress, the inflammatory response, repair liver function damage, and promote glycogen synthesis caused by T2DM. SA could also activate the PI3K/AKT/GLUT-2 signaling pathway, promote glucose metabolism gene expression, and maintain glucose homeostasis. Furthermore, 16S rRNA analysis revealed that SA could reduce the Firmicutes/Bacteroidota (F/B) ratio; promote norank_f__Muribaculaceae, Allobaculum, Akkermansia, and Eubacterium_siraeum_group proliferation; increase the levels of major short-chain fatty acids (SCFAs), such as acetic acid, propionic acid, and butyric acid; and maintain the homeostasis of the intestinal flora. In conclusion, these results suggested that SA could reshape the structural composition of intestinal microbes, activate the PI3K/AKT/GLUT2 pathway, improve insulin resistance, and decrease blood glucose levels.

Protective Effects of Shrimp Peptide on Dextran Sulfate Sodium-Induced Colitis in Mice.

Inflammatory bowel disease, an intestinal relapsing inflammatory disease, not only impairs gastrointestinal function but also increases the chances of developing colon cancer. Currently, the effects of shrimp peptide (SP) in mice model of ulcerative colitis (UC) are still unclear. In particular, it is uncertain whether SP affects the gut flora with UC mice. In this study, we investigated the anti-inflammatory effects of SP on a dextran sulfate sodium (DSS)-induced mouse model of UC. Firstly, the molecular weight of SP was mainly distributed in the range of 180-1,000 Da (61.95% proportion), and the amino acid composition showed that SP contained 17 amino acids, of which, the essential amino acids accounted for 54.50%. In vivo, oral SP significantly attenuated the severity of colitis, such as diarrhea, weight loss, and rectal bleeding. Furthermore, treatment with SP remarkably ameliorated intestinal barrier integrity, thus lowering the levels of the inflammatory cytokines and ameliorating antioxidant indices and intestinal injury indicators in the serum and colon. Lastly, the cecal contents were used to sequence and analyze the 16S rRNA genes of bacteria. Results suggested that treatment with SP could restore the balance of intestinal flora in modeled mice by regulating the abundance of pathogenic and beneficial bacteria. Furthermore, SP could significantly improve intestinal flora dysfunction in mice with UC. In summary, our findings show that SP has a prophylactic and therapeutic effect in UC in vivo, thereby highlighting its broad medicinal applications.

[Open arthrolysis for stiff knee after primary total knee arthroplasty].

Objective: To evaluate the effectiveness of open arthrolysis in treatment of the patient with stiff knee in late stage after primary total knee arthroplasty (TKA). Methods: Between January 2014 and October 2017, 7 female patients (7 knees) with stiff knee in late stage after primary TKA were admitted. The patients were 57-71 years old (mean, 63 years). There were 2 left knees and 5 right knees. All patients underwent TKA because of knee osteoarthritis. The interval between TKA and open arthrolysis was 8-30 months (mean, 13.6 months). There were 4 patients with 10-20° of extension deficit before arthrolysis. The range of motion of knee was (54.3±12.1)°. The clinical score, functional score, and total score of Knee Society Score (KSS) before arthrolysis were 76.3±7.6, 67.9±11.1, and 144.1±16.1, respectively. During the arthrolysis, periarticular soft tissue scar was removed, the range of motion of knee was restored, the gap balance and well patellar tracking were maintained. Intensive rehabilitation after operation was supplemented. Results: All wounds healed by first intention, without early stage complications. All patients were followed up 12-32 months with an average of 20.1 months. No abnormality of prosthesis was found by post-operative X-ray films. The knee movement improved significantly when compared with that before arthrolysis. The range of motion was less than 90° in 1 patient and 10° of extension deficit remained in 1 patient after operation. The range of motion was (92.9±4.9)° at last follow-up. The clinical score, functional score, and total score of KSS were 81.9±5.1, 74.3±9.8, and 156.1±13.7, respectively at last follow-up. The above indexes were superior to those before operation ( P<0.05). Conclusion: Open arthrolysis combined with intensive rehabilitation is a significant way to improve knee function for the patient with stiff knee in late stage after primary TKA.

Radixin enhances colon cancer cell invasion by increasing MMP-7 production via Rac1-ERK pathway.

As a member of the ezrin-radixin-moesin (ERM) family, radixin is overexpressed in many tumor tissues. However, little is known about its role in the progression of colon cancer. So we here aimed to determine the function of radixin in colon cancer cell invasion. Interestingly, we found that the expression of radixin was significantly elevated in colon cancer cells. Knockdown of radixin suppressed the invasion and migration of colon cancer cells. Further, knockdown of radixin inhibited the activation of Rac1 and ERK1/2, and decreased the expression and secretion of MMP-7. In addition, Rac1-ERK signaling pathway was required for the radixin-promoted invasion and MMP-7 production. Together, our findings suggest that radixin enhances the invasion and migration of colon cancer cells. Activation of Rac1-ERK pathway and consequent upregulation of MMP-7 production may contribute to the function of radixin in the regulation of colon cancer cell invasion. Thus, radixin may act as a novel target for the diagnosis and treatment of colon cancer.