Comparative Metabolic Profiling of Different Colored Rice Grains Reveals the Distribution of Major Active Compounds and Key Secondary Metabolites in Green Rice.

Pigmented rice grains are important resources for health and nutritional perspectives. Thus, a thorough dissection of the variation of nutrients and bioactive metabolites in different colored rice is of global interest. This study applied LC-MS-based widely targeted metabolite profiling and unraveled the variability of metabolites and nutraceuticals in long grain/non-glutinous black (BR), red (RR), green (GR), and white rice (WR) grains. We identified and classified 1292 metabolites, including five flavonoid compounds specific to BR. The metabolite profiles of the four rice grains showed significant variation, with 275-543 differentially accumulated metabolites identified. Flavonoid (flavone, flavonol, and anthocyanin) and cofactor biosynthesis were the most differentially regulated pathways among the four rice types. Most bioactive flavonoids, anthocyanidins (glycosylated cyanidins and peonidins), phenolic acids, and lignans had the highest relative content in BR, followed by RR. Most alkaloids, amino acids and derivatives, lipids, and vitamins (B6, B3, B1, nicotinamide, and isonicotinic acid) had higher relative contents in GR than others. Procyanidins (B1, B2, and B3) had the highest relative content in RR. In addition, we identified 25 potential discriminatory biomarkers, including fagomine, which could be used to authenticate GR. Our results show that BR and RR are important materials for medicinal use, while GR is an excellent source of nutrients (amino acids and vitamins) and bioactive alkaloids. Moreover, they provide data resources for the science-based use of different colored rice varieties in diverse industries.

Melatonin Delays Arthritis Inflammation and Reduces Cartilage Matrix Degradation through the SIRT1-Mediated NF-κB/Nrf2/TGF-ß/BMPs Pathway.

Cartilage, a flexible and smooth connective tissue that envelops the surfaces of synovial joints, relies on chondrocytes for extracellular matrix (ECM) production and the maintenance of its structural and functional integrity. Melatonin (MT), renowned for its anti-inflammatory and antioxidant properties, holds the potential to modulate cartilage regeneration and degradation. Therefore, the present study was devoted to elucidating the mechanism of MT on chondrocytes. The in vivo experiment consisted of three groups: Sham (only the skin tissue was incised), Model (using the anterior cruciate ligament transection (ACLT) method), and MT (30 mg/kg), with sample extraction following 12 weeks of administration. Pathological alterations in articular cartilage, synovium, and subchondral bone were evaluated using Safranin O-fast green staining. Immunohistochemistry (ICH) analysis was employed to assess the expression of matrix degradation-related markers. The levels of serum cytokines were quantified via Enzyme-linked immunosorbent assay (ELISA) assays. In in vitro experiments, primary chondrocytes were divided into Control, Model, MT, negative control, and inhibitor groups. Western blotting (WB) and Quantitative RT-PCR (q-PCR) were used to detect Silent information regulator transcript-1 (SIRT1)/Nuclear factor kappa-B (NF-κB)/Nuclear factor erythroid-2-related factor 2 (Nrf2)/Transforming growth factor-beta (TGF-ß)/Bone morphogenetic proteins (BMPs)-related indicators. Immunofluorescence (IF) analysis was employed to examine the status of type II collagen (COL2A1), SIRT1, phosphorylated NF-κB p65 (p-p65), and phosphorylated mothers against decapentaplegic homolog 2 (p-Smad2). In vivo results revealed that the MT group exhibited a relatively smooth cartilage surface, modest chondrocyte loss, mild synovial hyperplasia, and increased subchondral bone thickness. ICH results showed that MT downregulated the expression of components related to matrix degradation. ELISA results showed that MT reduced serum inflammatory cytokine levels. In vitro experiments confirmed that MT upregulated the expression of SIRT1/Nrf2/TGF-ß/BMPs while inhibiting the NF-κB pathway and matrix degradation-related components. The introduction of the SIRT1 inhibitor Selisistat (EX527) reversed the effects of MT. Together, these findings suggest that MT has the potential to ameliorate inflammation, inhibit the release of matrix-degrading enzymes, and improve the cartilage condition. This study provides a new theoretical basis for understanding the role of MT in decelerating cartilage degradation and promoting chondrocyte repair in in vivo and in vitro cultured chondrocytes.

Effect of Composite Probiotics on Antioxidant Capacity, Gut Barrier Functions, and Fecal Microbiome of Weaned Piglets and Sows.

This study investigated the efficacy of a composite probiotics composed of lactobacillus plantarum, lactobacillus reuteri, and bifidobacterium longum in alleviating oxidative stress in weaned piglets and pregnant sows. Evaluations of growth, oxidative stress, inflammation, intestinal barrier, and fecal microbiota were conducted. Results showed that the composite probiotic significantly promoted average daily gain in piglets (p < 0.05). It effectively attenuated inflammatory responses (p < 0.05) and oxidative stress (p < 0.05) while enhancing intestinal barrier function in piglets (p < 0.01). Fecal microbiota analysis revealed an increase in the abundance of beneficial bacteria such as faecalibacterium, parabacteroides, clostridium, blautia, and phascolarctobacterium in piglet feces and lactobacillus, parabacteroides, fibrobacter, and phascolarctobacterium in sow feces, with a decrease in harmful bacteria such as bacteroides and desulfovibrio in sow feces upon probiotic supplementation. Correlation analysis indicated significant negative associations of blautia with inflammation and oxidative stress in piglet feces, while treponema and coprococcus showed significant positive associations. In sow feces, lactobacillus, prevotella, treponema, and CF231 exhibited significant negative associations, while turicibacter showed a significant positive association. Therefore, the composite probiotic alleviated oxidative stress in weaned piglets and pregnant sows by modulating fecal microbiota composition.

Haplotype-resolved gapless genome and chromosome segment substitution lines facilitate gene identification in wild rice.

The abundant genetic variation harbored by wild rice (Oryza rufipogon) has provided a reservoir of useful genes for rice breeding. However, the genome of wild rice has not yet been comprehensively assessed. Here, we report the haplotype-resolved gapless genome assembly and annotation of wild rice Y476. In addition, we develop two sets of chromosome segment substitution lines (CSSLs) using Y476 as the donor parent and cultivated rice as the recurrent parents. By analyzing the gapless reference genome and CSSL population, we identify 254 QTLs associated with agronomic traits, biotic and abiotic stresses. We clone a receptor-like kinase gene associated with rice blast resistance and confirm its wild rice allele improves rice blast resistance. Collectively, our study provides a haplotype-resolved gapless reference genome and demonstrates a highly efficient platform for gene identification from wild rice.

A wild rice CSSL population facilitated identification of salt tolerance genes and rice germplasm innovation.

Salt stress is one of the major factors that limits rice production. Therefore, identification of salt-tolerant alleles from wild rice is important for rice breeding. In this study, we constructed a set of chromosome segment substitution lines (CSSLs) using wild rice as the donor parent and cultivated rice Nipponbare (Nip) as the recurrent parent. Salt tolerance germinability (STG) was evaluated, and its association with genotypes was determined using this CSSL population. We identified 17 QTLs related to STG. By integrating the transcriptome and genome data, four candidate genes were identified, including the previously reported AGO2 and WRKY53. Compared with Nip, wild rice AGO2 has a structure variation in its promoter region and the expression levels were upregulated under salt treatments; wild rice WRKY53 also has natural variation in its promoter region, and the expression levels were downregulated under salt treatments. Wild rice AGO2 and WRKY53 alleles have combined effects for improving salt tolerance at the germination stage. One CSSL line, CSSL118 that harbors these two alleles was selected. Compared with the background parent Nip, CSSL118 showed comprehensive salt tolerance and higher yield, with improved transcript levels of reactive oxygen species scavenging genes. Our results provided promising genes and germplasm resources for future rice salt tolerance breeding.

Bifidobacterium longum GL001 alleviates rat intestinal ischemia-reperfusion injury by modulating gut microbiota composition and intestinal tissue metabolism.

Intestinal ischemia-reperfusion (IIR) injury leads to inflammation and oxidative stress, resulting in intestinal barrier damage. Probiotics, due to their anti-inflammatory and antioxidant properties, are considered for potential intervention to protect the intestinal barrier during IIR injury. Bifidobacterium longum, a recognized probiotic, has targeted effects on IIR injury, but its mechanisms of action are not yet understood. To investigate the mechanism of Bifidobacterium longum intervention in IIR injury, we conducted a study using a rat IIR injury model. The results showed that Bifidobacterium longum could alleviate inflammation and oxidative stress induced by IIR injury by suppressing the NF-κB inflammatory pathway and activating the Keap1/Nrf2 signaling pathway. Bifidobacterium longum GL001 also increased the abundance of the gut microbiota such as Oscillospira, Ouminococcus, Corynebacterium, Lactobacillus, and Akkermansia, while decreasing the abundance of Allobaculum, [Prevotella], Bacteroidaceae, Bacteroides, Shigella, and Helicobacter. In addition, Bifidobacterium longum GL001 reversed the changes in amino acids and bile acids induced by IIR injury and reduced the levels of DL-cysteine, an oxidative stress marker, in intestinal tissue. Spearman correlation analysis showed that L-cystine was positively correlated with Lactobacillus and negatively correlated with Shigella, while DL-proline was positively correlated with Akkermansia. Moreover, bile acids, cholic acid and lithocholic acid, were negatively correlated with Lactobacillus and positively correlated with Shigella. Therefore, Bifidobacterium longum GL001 may alleviate IIR injury by regulating the gut microbiota to modulate intestinal lipid peroxidation and bile acid metabolism.

Lactiplantibacillus plantarum GL001 alleviates jejunal oxidative damage induced by intestinal ischemia-reperfusion injury by influencing jejunal tissue metabolism through the improvement of jejunal microbial composition.

Intestinal ischemia-reperfusion (IIR) injury is associated with inflammation and oxidative stress, yet its precise mechanisms remain not fully understood. IIR injury is closely linked to the gut microbiota and its metabolites. The anti-inflammatory and antioxidant effects of Lactiplantibacillus plantarum are specific to IIR. In our study, we conducted a 30-day pre-treatment of SD rats with both a standard strain of Lactiplantibacillus plantarum and Lactiplantibacillus plantarum GL001. After a 7-day cessation of treatment, we induced an IIR injury model to investigate the mechanisms by which Lactiplantibacillus plantarum alleviates IIR damage. The results demonstrate that Lactiplantibacillus plantarum effectively mitigates the inflammatory and oxidative stress damage induced by IIR. Lactiplantibacillus plantarum GL001 can improve the gut microbiota by reducing the abundance of harmful bacteria and increasing the abundance of beneficial bacteria. In IIR intestinal tissue, the levels of secondary bile acids are elevated. The content of the bacterial metabolite Calcimycin increases. Annotations of metabolic pathways suggest that Lactiplantibacillus plantarum GL001 can alleviate IIR damage by modulating calcium-phosphorus homeostasis through the regulation of parathyroid hormone synthesis, secretion, and action. Microbiota-metabolite correlation analysis reveals a significant negative correlation between calcimycin and Lactonacillus and a significant positive correlation between calcimycin and Shigella. There is also a significant positive correlation between calcimycin and secondary bile acids. Lactiplantibacillus plantarum GL001 can alleviate oxidative damage induced by IIR through improvements in gut microbiota and intestinal tissue metabolism.

Endoplasmic reticulum stress mediated by ROS participates in cadmium exposure-induced MC3T3-E1 cell apoptosis.

Cadmium (Cd), as one of the seventh most toxic heavy metal pollutants, widely persisted in the environment, leading to osteoblast dysfunction and ultimately Cd-related skeletal disease. However, the damaging effects of Cd on cellular functions and the potential pathogenic mechanisms are still unclear. In our study, Cd is believed to induce mitochondrial dysfunction and endoplasmic reticulum stress (ERS) in a dose-dependent manner, thereby leading to apoptosis, as evident by elevated Drp1, Fis1, GRP78, CHOP, ATF4, P-EIF2α, P-PERK, BAX, cleaved caspase 3 proteins expression and ROS levels, and decreased the levels of Mfn2, OPA1, Bcl2, and intracellular Collagen I, B-ALP, RUNX2, and BGP genes. Additionally, when the exogenous addition of NAC and 4-PBA was added, it was found that NAC and 4-PBA had a positive moderating effect on Cd-induced cell dysfunction. Mechanistically, Cd-induced oxidative stress and apoptosis by upregulating the PERK-EIF2α-ATF4-CHOP signaling pathway and inhibiting the Nrf2/NQO1 pathway. In conclusion, we found that Cd was involved in mitochondrial dysfunction, ERS, and apoptosis in MC3T3-E1 cells, While NAC and 4-PBA relieved ERS and attenuated cell apoptosis.

Oral administration of live combined Bacillus subtilis and Enterococcus faecium alleviates colonic oxidative stress and inflammation in osteoarthritic rats by improving fecal microbiome metabolism and enhancing the colonic barrier.

Osteoarthritis (OA) causes intestinal damage. The protective effect of probiotics on the intestine is indeed effective; however, the mechanism of protection against intestinal damage in OA is not clear. In this study, we used meniscal/ligamentous injury (MLI) to mimic OA in rats and explored the colonic protective effects of Bacillus subtilis and Enterococcus faecium on OA. Our study showed that treatment with B. subtilis and E. faecium attenuated colonic injury and reduced inflammatory and oxidative stress factors in the serum of osteoarthritic rats. α- and ß diversity of the fecal flora were not different among groups; no significant differences were observed in the abundances of taxa at the phylum and genus levels. We observed the presence of the depression-related genera Alistipes and Paraprevotella. Analysis of fecal untargeted metabolism revealed that histamine level was significantly reduced in the colon of OA rats, affecting intestinal function. Compared to that in the control group, the enriched metabolic pathways in the OA group were primarily for energy metabolisms, such as pantothenate and CoA biosynthesis, and beta-alanine metabolism. The treatment group had enriched linoleic acid metabolism, fatty acid biosynthesis, and primary bile acid biosynthesis, which were different from those in the control group. The differences in the metabolic pathways between the treatment and OA groups were more evident, primarily in symptom-related metabolic pathways such as Huntington's disease, spinocerebellar ataxia, energy-related central carbon metabolism in cancer, pantothenate and CoA biosynthesis metabolic pathways, as well as some neurotransmission and amino acid transport, and uptake- and synthesis-related metabolic pathways. On further investigation, we found that B. subtilis and E. faecium treatment enhanced the colonic barrier of OA rats, with elevated expressions of tight junction proteins occludin and Zonula occludens 1 and MUC2 mRNA. Intestinal permeability was reduced, and serum LPS levels were downregulated in the treatment group. B. subtilis and E. faecium also regulated the oxidative stress pathway Keap1/Nrf2, promoted the expression of the downstream protective proteins HO-1 and Gpx4, and reduced intestinal apoptosis. Hence, B. subtilis and E. faecium alleviate colonic oxidative stress and inflammation in OA rats by improving fecal metabolism and enhancing the colonic barrier.

Melatonin Prevents Chondrocyte Matrix Degradation in Rats with Experimentally Induced Osteoarthritis by Inhibiting Nuclear Factor-κB via SIRT1.

Osteoarthritis (OA) is a common degenerative joint disease characterized by an imbalance of cartilage extracellular matrix (ECM) breakdown and anabolism. Melatonin (MT) is one of the hormones secreted by the pineal gland of the brain and has anti-inflammatory, antioxidant, and anti-aging functions. To explore the role of MT in rats, we established an OA model in rats by anterior cruciate ligament transection (ACLT). Safranin O-fast green staining showed that intraperitoneal injection of MT (30 mg/kg) could alleviate the degeneration of articular cartilage in ACLT rats. Immunohistochemical (IHC) analysis found that MT could up-regulate the expression levels of collagen type II and Aggrecan and inhibit the expression levels of matrix metalloproteinase-3 (MMP-3), matrix metalloproteinase-13 (MMP-13), and ADAM metallopeptidase with thrombospondin type 1 motif 4 (ADAMTS-4) in ACLT rats. To elucidate the mechanism of MT in protecting the ECM in inflammatory factor-induced rat chondrocytes, we conducted in vitro experiments by co-culturing MT with a culture medium. Western blot (WB) showed that MT could promote the expression levels of transforming growth factor-beta 1 (TGF-ß1)/SMAD family member 2 (Smad2) and sirtuin 2-related enzyme 1 (SIRT1) and inhibit the expression of levels of phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibi-tor (p-p65) and phosphorylated IκB kinase-α (p-IκBα). In addition, WB and real-time PCR (qRT-PCR) results showed that MT could inhibit the expression levels of MMP-3, MMP-13, ADAMTS-4, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in chondrocytes induced by interleukin-1ß (IL-1ß), and up-regulate the expression of chondroprotective protein type II collagen. We found that in vivo, MT treatment protected articular cartilage in the rat ACLT model. In IL-1ß-induced rat chondrocytes, MT could reduce chondrocyte matrix degradation by up-regulating nuclear factor-kB (NF-κB) signaling pathway-dependent expression of SIRT1 and protecting chondrocyte by activating the TGF-ß1/Smad2 pathway.

Dark-light cycle disrupts bone metabolism and suppresses joint deterioration in osteoarthritic rats.

BACKGROUND: Light alteration affects the internal environment and metabolic homeostasis of the body through circadian rhythm disorders (CRD). CRD is one of the factors that induce and accelerate osteoarthritis (OA). Therefore, the aim of this study was to evaluate the effects of continuous dark-light (DL) cycle on joint inflammation, bone structure, and metabolism in normal and OA Sprague-Dawley (SD) rats. METHODS: Interleukin (IL)-1ß, IL-6, inducible nitric oxide synthase (iNOS), and tumor necrosis factor (TNF)-α were used to evaluate the systemic inflammation in rats. The pathological changes and inflammatory reactions of the cartilage and synovium of the knee joint in rats were evaluated by Safranin O-fast green and immunological staining. Bone turnover was assessed by histomorphometry and µCT scanning, as well as bone metabolism markers and proteins. The expression changes of clock proteins BMAL1, NR1D1, PER3, and CRY1 in representative tissues were detected by western blotting. RESULTS: DL cycle significantly inhibited body weight gain in normal and OA rats. The levels of proinflammatory factors in the peripheral blood circulation and degradation enzymes in the cartilage were significantly decreased in OA+DL rats. DL cycle significantly destroyed the structure of subchondral bone in hindlimbs of OA rats and reduced trabecular bone numbers. The decrease of bone mineral density (BMD), percent bone volume with respect to total bone volume (BV/TV), trabecular number (TB.N), osteoclast number, and mineralization could also be found. The ratio of the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin (RANKL/OPG) in the bone marrow of OA rats was markedly increased under DL, along with the activation of the mononuclear/phagocyte system. The expression of representative clock proteins and genes BMAL1, PER3, and CRY1 were markedly changed in the tissues of OA+DL rats. CONCLUSIONS: These results suggested that DL cycle dampened the arthritis and promoted bone resorption and bone mass loss. DL cycle affects bone turnover by regulating osteoclast production in osteoarthritic rats.

Xylazole inhibits NO-cGMP pathway in fetal rat nerve cells.

BACKGROUND: Xylazole (Xyl) is a veterinary anesthetic that is structurally and functionally similar to xylazine. However, the effects of Xyl in vitro remain unknown. OBJECTIVES: This study aimed to investigate the anesthetic mechanism of Xyl using fetal rat nerve cells treated with Xyl. METHODS: Fetal rat nerve cells cultured for seven days were treated with 10, 20, 30, and 40 µg/ mL Xyl for 0, 5, 10, 15, 20, 25, 30, 45, 60, 90, and 120 min. Variations of amino acid neurotransmitters (AANTs), Nitric oxide-Cyclic GMP (NO-cGMP) signaling pathway, and ATPase were evaluated. RESULTS: Xyl decreased the levels of cGMP and NO in nerve cells. Furthermore, Xyl affected the AANT content and Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity in nerve cells. These findings suggested that Xyl inhibited the NO-cGMP signaling pathway in nerve cells in vitro. CONCLUSIONS: This study provided new evidence that the anesthetic and analgesic effects of Xyl are related to the inhibition of the NO-cGMP signaling pathway.

Transgenic double-stranded RNA rice, a potential strategy for controlling striped stem borer (Chilo suppressalis).

BACKGROUND: Although the striped stem borer (SSB, Chilo suppressalis Walker) is a devastating pest of rice that causes significant economic losses, management options are currently limited. Plant-mediated RNA interference (RNAi) is an emerging crop protection technique in which transgenic plants are modified to express insect-specific double-stranded RNAs (dsRNAs) that trigger RNAi silencing in target pests. RESULT: In this study, an RNAi-based screen of 35 candidate SSB genes identified a small heat shock protein gene (CssHsp) as a potential plant-based RNAi target. To assess its utility in planta, a total of 39 transgenic rice plants were generated, with 11 independent transformants found to contain a single copy of the dsCssHsp expression cassette. In life-time feeding bioassays, three transgenic lines (DS10, DS35, DS36) were found to have significant negative impacts on SSB populations. After feeding for 8 days, mortality in the three transgenic lines exceeded 60%. By pupation, mortality further increased to 90% and few SSB survived to eclosion. Gene expression analyses confirmed that CssHsp transcript levels were significantly reduced after feeding on the transgenic dsCssHsp rice. CONCLUSION: These results demonstrate the potential for developing a plant-mediated RNAi strategy targeting CssHsp as a more biorational field-based approach for SSB control. © 2021 Society of Chemical Industry.

Chronic Circadian Rhythm Disturbance Accelerates Knee Cartilage Degeneration in Rats Accompanied by the Activation of the Canonical Wnt/ß-Catenin Signaling Pathway.

With the gradual deepening of understanding of systemic health and quality of life, the factors affecting osteoarthritis (OA) are not limited to mechanical injury, metabolic abnormality, age and obesity, etc., but circadian rhythm, which plays a non-negligible role in human daily life. The purpose of this study was to explore the molecular mechanism of chronic circadian rhythm disturbance (CRD) inducing cartilage OA-like degeneration. Rats with the anterior cruciate ligament excision transection (ACLT) were used to establish the early-stage OA model (6-week). The light/dark (LD) cycle shifted 12 h per week for 22 weeks in order to establish a chronic CRD model. BMAL1 knockdown (KD) and Wnt/ß-catenin pathway inhibition were performed in chondrocytes. The contents of proinflammatory factors and OA biomarkers in serum and chondrocyte secretions were detected by ELISA. Pathological and immunohistochemical staining of articular cartilage indicated the deterioration of cartilage. WB and qPCR were used to evaluate the relationship between matrix degradation and the activation of Wnt/ß-catenin signaling pathway in chondrocytes. We found that chronic CRD could cause OA-like pathological changes in knee cartilage of rats, accelerating cartilage matrix degradation and synovial inflammation. The expression of MMP-3, MMP-13, ADAMTS-4, and ß-catenin increased significantly; BMAL1, Aggrecan, and COL2A1 decreased significantly in either LD-shifted cartilage or BMAL1-KD chondrocytes. The expression of ß-catenin and p-GSK-3ß elevated, while p-ß-catenin and GSK-3ß diminished. The inhibitor XAV-939 was able to mitigated the increased inflammation produced by transfected siBMAL1. Our study demonstrates that chronic CRD disrupts the balance of matrix synthesis and catabolic metabolism in cartilage and chondrocytes, and it is related to the activation of the canonical Wnt/ß-catenin signaling pathway.

Emodin protects knee joint cartilage in rats through anti-matrix degradation pathway: An in vitro and in vivo study.

AIMS: Osteoarthritis (OA) is a common joint disease and the main cause of disability. We sought to determine the effective concentration of emodin on chondrocytes and to identify the dosage of emodin that induces a comparable therapeutic effect with the COX-2 inhibitor drug, celecoxib that is currently used to treat OA. MATERIAL AND METHODS: In vitro experiments induced inflammation of chondrocytes by IL-1ß, and an osteoarthritis model was established in vivo by cutting rat anterior cruciate ligament. Western Blot, Real-time PCR, HE staining, Safranin O-green staining and immunohistochemistry were performed to detect MMP-3, MMP-13, ADAMTS-4, iNOS and COL2A1 on the chondrocytes or the tibial plateau. The cytokine activity and content in serum of six groups of rats were measured by kit. RESULTS: It was found that the surface layer of the cartilage was thicker and smoother after the administration of emodin. Tissue expression of MMP-3, MMP-13, ADAMTS-4 and iNOS were significantly (p < 0.05) decreased in chondrocytes and cartilage treated with different doses of emodin, and the content of COL2A1 was reversed. Emodin also significantly decreased the blood levels of COX-2 and PGE2. The effective emodin in vitro was 5 µmol/L, whereas emodin at 80 mg/kg was equivalent to celecoxib in vivo. CONCLUSION: Emodin reduces the expression of cartilage matrix degradation biomarkers, thereby reducing the degradation of cartilage matrix and protecting the knee joint cartilage. Emodin at 5 µmol/L shows the best concentration to treat chondrocytes, and the protective effect of emodin at 80 mg/kg is comparable to that of celecoxib.

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix-degrading pathways in osteoarthritis-induced rat model.

Puerarin is an isoflavone isolated from the medicinal plant Pueraria lobata. The purpose of this study was to study the antiinflammatory and antimatrix-degrading effects of puerarin in a rat osteoarthritis (OA) model and its protective effects on joints. The rat OA model was established by anterior cruciate ligament transection (ACLT) surgery. Rats (n = 40) were divided into nontreated OA, OA + celecoxib (2.86 mg/kg), OA + puerarin (50 and 100 mg/kg), and control groups. Two weeks after surgical induction, puerarin was administered by gavage daily for 8 weeks. After 8 weeks, macroscopic observation and histopathological images showed that cartilage damage was reduced after puerarin and celecoxib treatment, the intensity of Safranin O staining was high, and the OARSI scores were significantly reduced compared to the OA group. Puerarin reduced the expression of MMP-3, MMP-13, ADAMTS-5, and COX-2 in the cartilage tissue of ACLT rats, inhibited the production of IL-1ß, IL-6, and TNF-α inflammatory factors, increased Type II collagen content, and altered the expression of serum OA cartilage degradation/bone turnover biomarkers (CTX-I, CTX-II, COMP, and PIINP). Based on these findings, we speculate that puerarin supplement to attain recovery from OA damage.

OsMYB3 is a R2R3-MYB gene responsible for anthocyanin biosynthesis in black rice.

Black rice is a rare type of rice germplasm with various health benefits that are largely attributed to anthocyanin pigment accumulation in the pericarps. The anthocyanin biosynthesis in plant tissues is activated mainly by the MBW complexes, consisting of three types of transcription factors R2R3-MYB, bHLH, and WDR. In black rice, the bHLH and WDR components regulating anthocyanin biosynthesis in pericarps have been characterized, while the R2R3-MYB factor remains unknown. By examining the expression correlation between all putative rice MYB genes and anthocyanin biosynthesis-related genes based on transcriptome data of pericarps in combination with further molecular and genetic analysis, we proved that OsMYB3 (LOC_Os03g29614) was the determinant R2R3-MYB gene for anthocyanin biosynthesis in rice pericarps. The expression level of OsMYB3 in pericarps of black rice was significantly higher than that of white rice. The knockout of OsMYB3 in a black rice variety caused significant downregulation of 19 anthocyanin metabolites and many other flavonoids in grains. Our research deepens the understanding of regulatory system for anthocyanin biosynthesis in rice pericarps and provides implications for breeding black rice varieties with high anthocyanin level. Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-021-01244-x.

Prospects of circadian clock in joint cartilage development.

Altering the food intake, exercise, and sleep patterns have a great influence on the homeostasis of the biological clock. This leads to accelerated aging of the articular cartilage, susceptibility to arthropathy and other aspects. Deficiency or overexpression of certain circadian clock-related genes accelerates the cartilage deterioration and leads to phenotypic variation in different joints. The process of joint cartilage development includes the formation of joint site, interzone, joint cavitation, epiphyseal ossification center, and cartilage maturation. The mechanism by which, biological clock regulates the cell-cycle, growth, metabolism, and other biological processes of chondrocytes is poorly understood. Here, we summarized the interaction between biological clock proteins and developmental pathways in chondrogenesis and provided the evidence from other tissues that further predicts the molecular patterns of these protein-protein networks in activation, proliferation, and differentiation. The purpose of this review is to gain deeper understanding of the evolution of cartilage and its irreversibility seen in damage and aging.

Improving nutritional quality of rice for human health.

KEY MESSAGE: This review surveys rice nutritional value, mainly focusing on breeding achievements via adoption of both genetic engineering and non-transgenic strategies to improve key nutrients associated with human health. Rice (Oryza sativa) is an essential component of the diets and livelihoods of over 3.5 billion people. Polished rice is mostly consumed as staple food, fulfilling daily energy demands and part of the protein requirement. Brown rice is comparatively more nutritious, containing more lipids, minerals, vitamins, dietary fiber, micronutrients, and bioactive compounds. In this article, we review the nutritional facts about rice including the level of γ-aminobutyric acid, resistant starch, lysine, iron, zinc, ß-carotene, folate, anthocyanin, various carotenoids, and flavonoids, focusing on their synthesis and metabolism and the advances in their biofortification via adoption of both conventional and genetic engineering strategies. We conclude that besides representing a staple food, rice has the potential to become a source of various essential nutrients or bioactive compounds through appropriate genetic improvements to benefit human health and prevent certain chronic diseases. Finally, we discuss the available, non-genetically engineering strategies for the nutritional improvement of rice, including their main strengths and constraints.