Deteriorating complementary feeding practices and dietary quality in Jordan: Trends and challenges.

Quality complementary feeding (CF) of infants and young children is key to their growth and development. But in Jordan, providing appropriate CF remains a challenge. This study assesses trends in infant and young child feeding (IYCF) practices, and consumption by infants and young children aged 6-23 months of breast milk substitutes (BMSs), sugar-sweetened beverages (SSBs), and micronutrient-rich foods in Jordan from 1990 to 2017. We combined dietary data on infants and young children from six Demographic and Health Surveys (DHS) (n = 14,880 children) to compute IYCF indicators. The latter included minimum dietary diversity (MDD), minimum meal frequency (MMF), and minimum acceptable diet (MAD), as well as intake of micronutrient-rich foods and food groups, specific SSBs, and infant formula. We conducted trend analyses using logistic regression models adjusted for child's age in month, child age squared, governorates, urban/rural residence, mother's educational attainment, and household wealth quintiles. We found that the proportion of consumption of micronutrient-rich food groups declined significantly between 1990 and 2017, with fewer infants and young children consuming eggs (OR = 0.39, p ≤ 0.001, 2002 reference), meat, poultry, and fish (OR = 0.25, p ≤ 0.001, 2002 reference), dairy (OR = 0.59, p ≤ 0.001, 2002 reference) and Vitamin A-rich fruits and vegetables (OR = 0.66, p ≤ 0.001, 2002 reference). Conversely, there was increased use of BMSs and sugar-sweetened juices that paralleled a decline in the share of infants and young children meeting appropriate CF practices and consuming micronutrient-rich foods and food groups. By 2017, children aged 6-23 months were significantly less likely to meet MDD, MMF, and subsequently MAD; the odds of consuming BMSs were almost three times the reference (OR = 3.8, p ≤ 0.001, 1990 reference), as were the odds of consuming sugar sweetened juices  (OR = 3.63, p ≤ 0.001, 1990 reference). Food insecurity and undernutrition are low in Jordan; however, overweight and obesity rates are increasing concurrently as are micronutrient deficiencies. This highlights the need for policymakers to address factors at individual and household levels (behaviours and practices) as well as environmental issues (increasing access to unhealthy and ultraprocessed foods).

Mollugin prevents CLP-induced sepsis in mice by inhibiting TAK1-NF-κB/MAPKs pathways and activating Keap1-Nrf2 pathway in macrophages.

Sepsis is a life-threatening organ dysfunction associated with macrophage overactivation. Targeted therapy against macrophages is considered a promising strategy for sepsis treatment. Mollugin (MLG), a compound extracted from traditional Chinese medicine Rubia cordifolia L., possesses anti-tumor and anti-inflammatory activities. This study aimed to investigate the anti-inflammatory effects and mechanisms of MLG in macrophages and its therapeutic role in CLP-induced sepsis in mice. The results demonstrated that MLG downregulated the inflammatory response induced by LPS or tumor necrosis factor α (TNF-α) in macrophages. Mechanistically, MLG suppressed the phosphorylation of TAK1, the upstream modulator of IKKα/ß and MAPKs, thereby inhibiting the pro-inflammatory signaling transduction of NF-κB and MAPKs. Additionally, MLG also activated the Nrf2 antioxidant pathway, reducing intracellular reactive oxygen species. CETSA and molecular docking analyses revealed that MLG could effectively bind to TAK1 and Keap1, which may be involved in the inhibition of TAK1- NF-κB/MAPKs and activation of Nrf2 mediated by MLG. Animal study demonstrated that MLG ameliorated inflammatory injury of lung and liver in CLP-induced sepsis mice probably by reducing the levels of pro-inflammatory cytokines. Therefore, our study suggests that bi-directional roles of MLG in improving sepsis via blocking the TAK1-NF-κB/MAPKs and activating Nrf2 pathways, indicating its potential as a promising candidate drug for sepsis treatment.

Dietary glutathione supplementation attenuates oxidative stress and improves intestinal barrier in diquat-treated weaned piglets.

The aim of this study was to investigate the protective effects of glutathione (GSH) against oxidative stress and intestinal barrier disruption caused by diquat (an oxidative stress inducer) in weaned piglets. Twenty-four piglets were randomly assigned to four treatments with six pigs per treatment for an 18-d trial. Treatments were basal diet, basal diet + diquat challenge, 50 mg/kg GSH diets + diquat challenge and 100 mg/kg GSH diets + diquat challenge. On day 15, piglets in basal diet group and diquat-challenged groups were intraperitoneally injected with sterile saline and diquat at 10 mg/kg body weight, respectively. The results showed that GSH supplementation improved growth performance of diquat-injected piglets from days 15 to 18 (p < 0.05), especially at a dose of 100 mg/kg GSH. Meanwhile, diquat also caused oxidative stress and intestinal barrier damage in piglets. However, GSH supplementation enhanced the antioxidant capacity of serum and jejunum, as evidenced by the increase in GSH content and total superoxide dismutase activities and the decrease in 8-hydroxy-2'-deoxyguanosine concentrations (p < 0.05). GSH also up-regulated the mRNA expressions of intestinal tight junction protein (zonula occludens 1, ZO1; occludin, OCLN; claudin-1, CLDN1) and mitochondrial biogenesis and function (peroxisome proliferator-activated receptor-gamma coactivator-1 alpha, PGC1α; mitochondrial transcription factor A, TFAM; cytochrome c, CYCS), compared with diquat-challenged piglets in basal diet (p < 0.05). Thus, the study demonstrates that GSH protects piglets from oxidative stress caused by diquat and 100 mg/kg GSH has a better protective role.

Berberine Ameliorates Glucose Metabolism in Diabetic Rats through the alpha7 Nicotinic Acetylcholine Receptor-Related Cholinergic Anti-Inflammatory Pathway.

Berberine is an isoquinoline derivative alkaloid extracted from Chinese herbs. Recent studies have demonstrated the therapeutic effect of berberine on glucose metabolic disorders. However, its specific mechanism is still unclear. Our study aimed to research the glucose-lowering effect of berberine in diabetic rats and to reveal the possible role of the cholinergic anti-inflammatory pathway. Diabetic rats induced by administration of a high-calorie diet and streptozocin tail vein injection were assessed by the oral glucose tolerance test. Then, the diabetic rats were divided into two groups, those with or without the alpha7 nicotinic acetylcholine receptor gene downregulated, respectively, followed by treatment including berberine for 6 weeks. Results of this study show that the administration of berberine downregulated levels of fasting blood glucose and fasting insulin, and ameliorated insulin resistance in diabetic rats. Treatment with berberine inhibited acetylcholinesterase activity, and upregulated acetylcholine levels in the serum and alpha7 nicotinic acetylcholine receptor gene expression in the liver tissue. Meanwhile, berberine reversed elevated expression of cytokines interleukin-1ß and TNF-α in the serum and downregulated nuclear factor κB expression. However, berberine administration showed no glucose-lowering or anti-inflammatory effect in diabetic rats in which alpha7 nicotinic acetylcholine receptor gene expression was downregulated, and acetylcholinesterase activity was also significantly inhibited. In conclusion, berberine may ameliorate glucose metabolism by activating the alpha7 nicotinic acetylcholine receptor-mediated cholinergic anti-inflammatory pathway.

Jiao-tai-wan inhibits inflammation of the gut-brain-axis and attenuates cognitive impairment in insomnic rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Jiao-tai-wan is a well-known traditional Chinese herbal medicine formula that is used to treat insomnia and systemic inflammation. Studies indicate chronic insomnia might contribute to the prevalence of cognitive impairment. The role of systemic inflammation and intestinal permeability in the progression of neurodegenerative diseases attracts much attention. AIM OF THE STUDY: This study aimed to investigate if Jiao-tai-wan plays a role in promoting the repair of the intestinal epithelial barrier to suppress systemic inflammation and cognitive impairment in sleep-deprived (SD) rats. MATERIALS AND METHODS: Male obesity-resistant SD rats were partially sleep-deprived for 16 weeks. During the last 8 weeks, they were treated with Jiao-tai-wan. A Morris water maze was used to analyze their cognitive ability. Aß42 and proinflammation cytokines in the cerebrospinal fluid, tissue, or serum were determined using enzyme-linked immunosorbent assay or polymerase chain reaction. Intestinal permeability was detected using the fluorescein isothiocyanate-dextran perfusion assay method. Plasma lipopolysaccharide (LPS) levels were detected with Tachypleus Amebocyte Lysate. Western bolt was used in the signaling pathway analysis. RESULTS: Sleep deprivation deteriorated the performance of rats in the Morris water maze and increased the Aß42, caspase3, IL-6, and TNF-α levels in their brains. The intestinal TLR4/NF-κB pathway was activated with an increase in the expression of IL-6 and TNF-α. The expression of tight junction proteins was also decreased in the intestinal tissue. This increased the intestinal permeability and circulation of LPS, LPS binding protein, IL-6, and TNF-α. Treatment with Jiao-tai-wan could partly reverse these changes. CONCLUSION: Jiao-tai-wan has the potential to attenuate systemic inflammation and cognitive impairment in partially sleep-deprived rats. The possible underlying mechanism is by preventing an inflammation trigger being transferred through the gut-brain-axis.

Coptidis Rhizoma inhibits NLRP3 inflammasome activation and alleviates renal damage in early obesity-related glomerulopathy.

BACKGROUND: Obese subjects have been considered to be in a state of chronic, low-grade systemic inflammation. Excess fat accumulation and persistent inflammation may promote renal dysfunction, to cause chronic kidney disease (CKD) and even end-stage kidney failure. Coptidis Rhizoma is a classical traditional Chinese herb well known for its hypoglycemic and hypolipidemic properties. The mechanism is partially associated with its anti-inflammatory effect. However, this effect is rarely investigated in obesity and obesity-related glomerulopathy (ORG). PURPOSE: The current study was designed to evaluate the effect of Coptidis Rhizoma on ORG. It also aimed to determine whether this renal protection effect of Coptidis Rhizoma was related to the inhibition of NLRP3 inflammasome in ORG. METHODS: Coptidis Rhizoma concentrated granules were prepared and the main components were identified by 3D-High Performance Liquid Chromatography (3D-HPLC) assay. The animal model of early stage ORG was established in obesity-prone (OP) rats by high protein and high fat diet feeding for 12 weeks. The treatment with Coptidis Rhizoma at different dosages was administered by intragastric infusion simultaneously. Then body weight, kidney weight, plasma lipid profiles, 24 h urine protein/albumin content and kidney histology were measured. Inflammatory biomarkers were examined both in the rat plasma and renal cortex. The gene expressions of NLRP3 inflammasome complex and NF-κB in renal tissues were also measured. RESULTS: Coptidis Rhizoma alleviated dyslipidemia and reduced the renal weight of the rats with ORG. Meanwhile, urinary albumin to creatinine ratio and creatinine clearance rate were significantly improved. Coptidis Rhizoma also attenuated glomerular hypertrophy, mesangial hyperplasia, and effacement of podocyte foot in renal tissues of ORG rats. In addition, Coptidis Rhizoma intervention decreased the levels of proinflammatory cytokines (TNF-α, IL-1ß, IL-6, and IL-18) both in plasma and renal tissue. The gene expression of NLRP3 inflammasome was down-regulated and NF-κB activity was also inhibited by Coptidis Rhizoma in renal tissues of ORG rats. CONCLUSION: Coptidis Rhizoma can ameliorate early renal damage in ORG rats and the mechanisms appear to be related to the inhibition of NLRP3 inflammasome complex.

Jiao-tai-wan Up-regulates Hypothalamic and Peripheral Circadian Clock Gene Cryptochrome and Activates PI3K/AKT Signaling in Partially Sleep-deprived Rats.

This study aims to explore the effect and mechanism of Jiao-tai-wan (JTW) on systemic and tissue-specific inflammation and insulin resistance in obesity-resistant (OR) rats with chronic partial sleep deprivation (PSD). OR rats with PSD were orally given JTW and Estazolam for 4 weeks. The amount of food intake and metabolic parameters such as body weight increase rate, fasting plasma glucose (FPG), fasting insulin (FINS), homeostasis model assessment-insulin resistance (HOMA-IR) and plasma inflammatory markers were measured. The expression levels of circadian proteins cryptochrome 1 (Cryl) and cryptochrome 2 (Cry2) in hypothalamus, adipose and liver tissues were also determined. Meanwhile, the mRNA expression of inflammatory markers, activity of nuclear factor kappa B (NF-κB) p65 protein, as well as the expression levels of insulin signaling pathway proteins in hypothalamus, adipose and liver tissues were measured. Additionally, cyclic adenosine 3', 5'-monophosphate (cAMP) and activity of vasodilator-stimulated phosphoprotein (VASP) in hypothalamus tissue were measured. JTW significantly decreased the body weight increase rate and food intake, ameliorated systemic inflammation and insulin resistance. JTW effectively ameliorated inflammation and increased PI3K/AKT signaling activation in hypothalamus, adipose and liver. Interestingly, all these changes were associated with the up-regulation of circadian gene Cryl and Cry2 protein expression. We also found that in hypothalamus tissue of PSD rats, down-regulation of Cryl and Cry2 activated cAMP/PKA signaling and then led to inflammation, while JTW inhibited this signaling. These results suggested that JTW has the beneficial effect on ameliorating inflammation and insulin resistance in partially sleep-deprived rats by up-regulating Cry expression.

Effect of Jiaotai Pill () on intestinal damage in partially sleep deprived rats.

OBJECTIVE: To explore the effect and mechanism of Jiaotai Pill (, JTW) on intestinal mucosal damage in rats with chronic partial sleep deprivation (PSD). METHODS: Obesity resistant (OR) rats were selected, and underwent 4 h PSD by being exposed to environmental noise for 4 weeks. During the whole PSD period, JTW and estazolam were orally given to the rats respectively in the treating groups. Plasma concentration of lipopolysaccharide (LPS) which is the marker of gut-origin endotoxemia was examined. Intestinal morphology changes were observed by optical microscopy. The protein expression of occludin (Ocln) in the intestine was measured by immunofluorescence technique and Western blot. The expressions of circadian proteins cryptochromes (Cry1 and Cry2) in the intestine were also determined. RESULTS: The treatment of JTW significantly decreased LPS level in OR rats with PSD (P<0.05). JTW also attenuated insomnia-induced intestinal injury like shorter, sparse and incomplete villus, wide gap between the villus, mucosal swelling and congesting (P<0.05). These changes were associated with the effect of JTW on up-regulating the expressions of Cry1 protein, Cry2 protein and Ocln protein in the intestine. CONCLUSIONS: JTW has the beneficial effect on improving intestinal mucosal damage caused by PSD. The mechanism appears to be related to the modulation of the expressions of circadian proteins and Ocln protein in the intestine, thereby attenuating inflammation and improving insulin resistance in insomnia rats.

[Research progress of berberine in treatment of diabetic kidney disease].

Diabetic kidney disease (DKD) is a chronic renal microvascular complication associated with abnormal glucose metabolism, which is an important cause of end stage renal disease. Diabetes can damage the kidney through many ways, including renal vascular, glomerular, tubular, and renal interstitial damages. Therefore, a comprehensive treatment process must be taken for the treatment of DKD, and the selection of appropriate drugs has important significance in the treatment of DKD. Berberine has significant curative effect in the treatment of DKD, and the mechanism is related to the reduction of blood sugar, improvement of renal hemodynamics abnormality, regulation of blood lipid profile and the attenuation of systemic and local inflammation.