Stored white tea ameliorates DSS-induced ulcerative colitis in mice by modulating the composition of the gut microbiota and intestinal metabolites.

Changes in the chemical composition of white tea during storage have been studied extensively; however, whether such chemical changes impact the efficacy of white tea in ameliorating colitis remains unclear. In this study, we compared the effects of new (2021 WP) and 10-year-old (2011 WP) white tea on 3% dextrose sodium sulfate (DSS)-induced ulcerative colitis in mice by gavaging mice with the extracts at 200 mg kg-1 day-1. Chemical composition analysis showed that the levels of 50 compounds, such as flavanols, dimeric catechins, and amino acids, were significantly lower in the 2011 WP extract than in the 2021 WP extract, whereas the contents of 21 compounds, such as N-ethyl-2-pyrrolidinone-substituted flavan-3-ols, theobromine, and (-)-epigallocatechin-3-(3''-O-methyl) gallate, were significantly higher. Results of the animal experiments showed that 2011 WP ameliorated the pathological symptoms of colitis, which was superior to the activity of 2021 WP, and this effect was likely enhanced based on the decreasing of the relative abundance of the g_bacteroides and g_Escherichia-Shigella flora in mice with colitis and promoting the conversion of primary bile acids to secondary bile acids in the colon. These results will facilitate the development of novel functional products from white tea.

Evidence for chromium crosses blood brain barrier from the hypothalamus in chromium mice model.

It has been shown that exposure to hexavalent Chromium, Cr (Ⅵ), via nasal cavity can have neurotoxicological effects and induces behavioral impairment due to the fact that blood brain barrier (BBB) does not cover olfactory bulb. But whether Cr (Ⅵ) can cross the BBB and have a toxicological effects in central nervous system (CNS) remains unclear. Therefore, we investigated the effects of Cr (Ⅵ) on mice treated with different concentrations and exposure time (14 days and 28 days) of Cr (Ⅵ) via intraperitoneal injection. Results revealed that Cr accumulated in hypothalamus (HY) in a timely dependent manner. Much more severer neuropathologies was observed in the group of mice exposed to Cr (Ⅵ) for 28 days than that for 14 days. Gliosis, neuronal morphological abnormalities, synaptic degeneration, BBB disruption and neuronal number loss were observed in HY. In terms of mechanism, the Nrf2 related antioxidant stress signaling dysfunction and activated NF-κB related inflammatory pathway were observed in HY of Cr (Ⅵ) intoxication mice. And these neuropathologies and signaling defects appeared in a timely dependent manner. Taking together, we proved that Cr (Ⅵ) can enter HY due to weaker BBB in HY and HY is the most vulnerable CNS region to Cr (Ⅵ) exposure. The concentration of Cr in HY increased along with time. The accumulated Cr in HY can cause BBB disruption, neuronal morphological abnormalities, synaptic degeneration and gliosis through Nrf2 and NF-κB signaling pathway. This finding improves our understanding of the neurological dysfunctions observed in individuals who have occupational exposure to Cr (Ⅵ), and provided potential therapeutic targets to treat neurotoxicological pathologies induced by Cr (Ⅵ).

Carboxymethylated Abrus cantoniensis polysaccharide prevents CTX-induced immunosuppression and intestinal damage by regulating intestinal flora and butyric acid content.

As a Chinese folk health product, Abrus cantoniensis exhibits good immunomodulatory activity because of its polysaccharide components (ACP), and carboxymethylation of polysaccharides can often further improve the biological activity of polysaccharides. In this study, we explored the impact of prophylactic administration of carboxymethylated Abrus cantoniensis polysaccharide (CM-ACP) on immunosuppression and intestinal damage induced by cyclophosphamide (CTX) in mice. Our findings demonstrated that CM-ACP exhibited a more potent immunomodulatory activity compared to ACP. Additionally, CM-ACP effectively enhanced the abundance of short-chain fatty acid (SCFA)-producing bacteria in immunosuppressed mice and regulated the gene expression of STAT6 and STAT3 mediated pathway signals. In order to further explore the relationship among polysaccharides, intestinal immunity and intestinal flora, we performed a pseudo-sterile mouse validation experiment and fecal microbiota transplantation (FMT) experiment. The findings suggest that CM-FMT and butyrate attenuate CTX-induced immunosuppression and intestinal injury. CM-FMT and butyrate show superior immunomodulatory ability, and may effectively regulate intestinal cell metabolism and repair the damaged intestine by activating STAT6 and STAT3-mediated pathways. These findings offer new insights into the mechanisms by which CM-ACP functions as functional food or drug, facilitating immune response regulation and maintaining intestinal health.

Epigallocatechin gallate delays age-related cataract development via the RASSF2/AKT pathway.

Age-related cataract (ARC) is a common eye disease, the main cause of which is oxidative stress-mediated apoptosis of lens epithelial cells (LECs). Epigallocatechin gallate (EGCG) is the most potent antioxidant in green tea. Our results demonstrated that EGCG could effectively reduce apoptosis of LECs and retard lens clouding in aged mice. By comparing transcriptome sequencing results of three groups of mice (young control, untreated aged, and EGCG-treated) and screening using GO and KEGG analyses, we selected RASSF2 as the effector gene of EGCG for mechanistic exploration. We verified that the differential expression of RASSF2 was associated with the occurrence of ARC in clinical samples and mouse tissues by immunohistochemistry and western blotting, respectively. We showed that high RASSF2 expression plays a crucial role in the oxidative induction of apoptosis in LECs, as revealed by overexpression and interference experiments. Further studies showed that RASSF2 mediates the inhibitory effect of EGCG on apoptosis and ARCogenesis in LECs by regulating AKT (Ser473) phosphorylation. In this study, we found for the first time the retarding effect of EGCG on lens clouding in mice and revealed the mechanism of action of RASSF2/AKT in it, which provides a theoretical basis for the targeted treatment of EGCG.

Saponins from Panax japonicus improve neuronal mitochondrial injury of aging rats.

CONTEXT: Panax japonicus is the dried rhizome of Panax japonicus C.A. Mey. (Araliaceae). Saponins from Panax japonicus (SPJ) exhibit anti-oxidative and anti-aging effects. OBJECTIVE: We evaluated the neuroprotective effects of SPJ on aging rats. MATERIALS AND METHODS: Sprague-Dawley rats (18-months-old) were randomly divided into aging and SPJ groups (n = 8). Five-month-old rats were taken as the adult control (n = 8). The rats were fed a normal chow diet or the SPJ-containing diet (10 or 30 mg/kg) for 4 months. An in vitro model was established by d-galactose (d-Gal) in the SH-SY5Y cell line and pretreated with SPJ (25 and 50 µg/mL). The neuroprotection of SPJ was evaluated via Nissl staining, flow cytometry, transmission electron microscopy and Western blotting in vivo and in vitro. RESULTS: SPJ improved the neuronal degeneration and mitochondrial morphology that are associated with aging. Meanwhile, SPJ up-regulated the protein levels of mitofusin 2 (Mfn2) and optic atrophy 1 (Opa1) and down-regulated the protein level of dynamin-like protein 1 (Drp1) in the hippocampus of aging rats (p < 0.05 or p < 0.01 vs. 22 M). The in vitro studies also demonstrated that SPJ attenuated d-Gal-induced cell senescence concomitant with the improvement in mitochondrial function; SPJ, also up-regulated the Mfn2 and Opa1 protein levels, whereas the Drp1 protein level (p < 0.05 or p < 0.01 vs. d-Gal group) was down-regulated. DISCUSSION AND CONCLUSIONS: Further research on the elderly population will contribute to the development and utilization of SPJ for the treatment of neurodegenerative disorders.

Catechol-Modified and MnO2-Nanozyme-Reinforced Hydrogel with Improved Antioxidant and Antibacterial Capacity for Periodontitis Treatment.

Periodontitis is an inflammatory disease characterized by tooth loss and alveolar bone resorption. Bacteria are the original cause of periodontitis, and excess reactive oxygen species (ROS) encourage and intensify inflammation. In this study, a mussel-inspired and MnO2 NPs-reinforced adhesive hydrogel capable of alleviating periodontitis with improved antibacterial and antioxidant abilities was developed. The hydrogel was created by combining polyvinyl alcohol (PVA), 3,4-dihydroxy-d-phenylalanine (DOPA), and MnO2 nanoparticles (NPs) (named PDMO hydrogel). The hydrogel was demonstrated to be able to scavenge various free radicals (including total ROS─O2•- and OH•) and relieve the hypoxia in an inflammatory microenvironment by scavenging excess ROS and generating O2 due to its superoxide dismutase (SOD)/catalase (CAT)-like activity. Besides, under 808 nm near-infrared (NIR) light, the photothermal performance of the PDMO hydrogel displayed favorable antibacterial and antibiofilm effects toward Escherichia coli, Staphylococcus aureus, and Porphyromonas gingivalis (up to nearly 100% antibacterial rate). Furthermore, the PDMO hydrogel exhibited favorable therapeutic efficacy in alleviating gingivitis in Sprague-Dawley rats, even comparable to or better than the commercial PERIO. In addition, in the periodontitis models, the PDMO2 group showed the height of the residual alveolar bone and the smallest shadow area of low density among other groups, indicating the positive role of the PDMO2 hydrogel in bone regeneration. Finally, the biosafety of the PDMO hydrogel was comprehensively investigated, and the hydrogel was demonstrated to have good biocompatibility. Therefore, the developed PDMO hydrogel provided an effective solution to resolve biofilm recolonization and oxidative stress in periodontitis and could be a superior candidate for local drug delivery system in the clinical management of periodontitis with great potential for future clinical translation.

Long-term Pu-erh tea consumption improves blue light-induced depression-like behaviors.

Blue light emitted by smartphones and tablets at night increases the risk of depression. Pu-erh tea has been reported to reduce the risk of depression by regulating tryptophan metabolism, but its underlying protective mechanism on depression induced by blue light at night (BLAN) remains unclear. In this work, two groups of C57BL6/J mice were given water or 0.25% (w/v) Pu-erh tea for 120 days, followed by a 45-day BLAN treatment (400 lux blue light between 21:00 and 23:00) to simulate blue light emitted from electronic equipment. Our results indicated that BLAN induced depression-like behaviors and gut microbiota disorders in healthy mice. Pu-erh tea intake significantly reshaped the gut microbiome (especially Bifidobacterium) and regulated the metabolism of short-chain fatty acids (SCFAs) which protected the integrity of the intestinal barrier. This improvement further reduced blood-brain barrier (BBB) damage and alleviated neuroinflammation by inhibiting MyD88/NF-κB pathways which finally regulated neurotransmitters such as brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT). Collectively, 0.25% (w/v) Pu-erh tea has the potential to prevent BLAN-induced depression-like behaviors by reshaping the gut microbiota and increasing the generation of SCFAs via the gut-brain axis.

Pu-erh tea alleviated colitis-mediated brain dysfunction by promoting butyric acid production.

Brain inflammation develops with increased colitis. Pu-erh tea is considered a potential dietary intervention to improve colitis. However, it's unclear whether Pu-erh tea helps alleviate colitis-mediated brain dysfunction. Here, we found that colitis triggered brain dysfunction and increased the risk of depression. Pu-erh tea improved gut-brain barrier function (increased ZO-1 and Occludin) and restored short-chain fatty acids (SCFAs) as well as neurotransmitter release (γ-GABA, 5-HT, and dopamine), which stemmed from the production of butyric acid (BA). Pu-erh tea and BA promoted the production of SCFAs by reshaping the gut microbes (increased Lactobacillus, Akkermansia, Faecalibaculum), thereby downregulating gut inflammatory protein expression (PI3K/AKT/NF-κB). SCFAs, especially BA, intervened directly in the blood-brain barrier via the gut-brain axis to restore neurotransmitter release. Collectively, our results highlighted that increasing BA through Pu-erh tea consumption may be a key mechanism for improving colitis-mediated brain dysfunction by lowering gut inflammation and balancing gut microbe-gut-brain axis homeostasis. These results provide a promising step that might encourage further investigations of Pu-erh tea as a protective agent for brain function in colitis patients.

The chemistry, processing, and preclinical anti-hyperuricemia potential of tea: a comprehensive review.

Hyperuricemia is an abnormal purine metabolic disease that occurs when there is an excess of uric acid in the blood, associated with cardiovascular diseases, hypertension, gout, and renal disease. Dietary intervention is one of the most promising strategies for preventing hyperuricemia and controlling uric acid concentrations. Tea (Camellia sinensis) is known as one of the most common beverages and the source of dietary polyphenols. However, the effect of tea on hyperuricemia is unclear. Recent evidence shows that a lower risk of hyperuricemia is associated with tea intake. To better understand the anti-hyperuricemia effect of tea, this review first briefly describes the pathogenesis of hyperuricemia and the processing techniques of different types of tea. Next, the epidemiological and experimental studies of tea and its bioactive compounds on hyperuricemia in recent years were reviewed. Particular attention was paid to the anti-hyperuricemia mechanisms targeting the hepatic uric acid synthase, renal uric acid transporters, and intestinal microbiota. Additionally, the desirable intake of tea for preventing hyperuricemia is provided. Understanding the anti-hyperuricemia effect and mechanisms of tea can better utilize it as a preventive dietary strategy.HighlightsHigh purine diet, excessive alcohol/fructose consumption, and less exercise/sleep are the induction factors of hyperuricemia.Tea and tea compounds showed alleviated effects for hyperuricemia, especially polyphenols.Tea (containing caffeine or not) is not associated with a higher risk of hyperuricemia.Xanthine oxidase inhibition (reduce uric acid production), Nrf2 activation, and urate transporters regulation (increase uric acid excretion) are the potential molecular targets of anti-hyperuricemic effect of tea.About 5 g tea intake per day may be beneficial for hyperuricemia prevention.

Tea combats circadian rhythm disorder syndrome via the gut-liver-brain axis: potential mechanisms speculated.

Circadian rhythm is an intrinsic mechanism developed by organisms to adapt to external environmental signals. Nowadays, owing to the job and after-work entertainment, staying up late - Circadian rhythm disorders (CRD) are common. CRD is linked to the development of fatty liver, type 2 diabetes, and chronic gastroenteritis, which affecting the body's metabolic and inflammatory responses via multi-organ crosstalk (gut-liver-brain axis, etc.). However, studies on the mechanisms of multi-organ interactions by CRD are still weak. Current studies on therapeutic agents for CRD remain inadequate, and phytochemicals have been shown to alleviate CRD-induced syndromes that may be used for CRD-therapy in the future. Tea, a popular phytochemical-rich beverage, reduces glucolipid metabolism and inflammation. But it is immature and unclear in the mechanisms of alleviation of CRD-mediated syndrome. Here, we have analyzed the threat of CRD to hosts and their offspring' health from the perspective of the "gut-liver-brain" axis. The potential mechanisms of tea in alleviating CRD were further explored. It might be by interfering with bile acid metabolism, tryptophan metabolism, and G protein-coupled receptors, with FXR, AHR, and GPCR as potential targets. We hope to provide new perspectives on the role of tea in the prevention and mitigation of CRD.HighlightsThe review highlights the health challenges of CRD via the gut-liver-brain axis.CRD research should focus on the health effects on healthy models and its offspring.Tea may prevent CRD by regulating bile acid, tryptophan, and GPCR.Potential targets for tea prevention and mitigation of CRD include FXR, AHR and GPCR.A comprehensive assessment mechanism for tea in improving CRD should be established.

Polygonatum sibiricum ameliorated cognitive impairment of naturally aging rats through BDNF-TrkB signaling pathway.

Cognitive dysfunction is high in the elderly population and seriously affects the quality of life. Brain-derived neurotrophic factor (BDNF) is one of the key neurotrophic proteins, and activation of BDNF-TrkB is considered an effective strategy to improve cognitive dysfunction during aging. In this study, administration of polygonatum sibiricum (PS) for 5 months effectively ameliorates the cognitive function, improving the Nissl body state in cortex and hippocampus in aging rats. In addition, PS can improve the synaptic structure and increase the number of synapses. Furthermore, PS reverses the reduction of synaptic plasticity-related proteins postsynaptic density protein 95 (PSD-95) and synaptophysin during aging and up-regulates the expression of BDNF-TrkB. In conclusion, PS improves cognitive dysfunction and enhances synaptic plasticity in naturally aged rats by regulating the BDNF-TrkB signaling pathway. PS has the potential to be developed as a novel and promising functional health food for the elderly. PRACTICAL APPLICATIONS: Polygonatum sibiricum (PS) is a traditional Chinese medicine, which has been included in the homologous plant of medicine and food. PS has been widely used to treat lung diseases, diabetes and antiaging in clinical. Studies have confirmed that PS can accelerate the repair and regeneration of damaged neurons, reverse the changes in synaptic structure, and improve the ability of learning and memory. Our study confirmed that PS significantly improved the cognitive function in aging rats. PS has great potential to be developed as a functional food for improving neurological function and anti-aging.

Hawk Tea Flavonoids as Natural Hepatoprotective Agents Alleviate Acute Liver Damage by Reshaping the Intestinal Microbiota and Modulating the Nrf2 and NF-κB Signaling Pathways.

Hawk tea (Litsea coreana Levl. var. lanuginosa) is a traditional herbal tea in southwestern China, and was found to possess hepatoprotective effects in our previous study. However, it is unclear whether hawk tea flavonoids (HTF) can alleviate alcoholic liver damage (ALD). Firstly, we extracted and identified the presence of 191 molecules categorized as HTFs, with reynoutrin, avicularin, guaijaverin, cynaroside, and kaempferol-7-O-glucoside being the most prevalent. After taking bioavailability into consideration and conducting comprehensive sorting, the contribution of guaijaverin was the highest (0.016 mg/mice). Then, by daily intragastric administration of HTF (100 mg/kg/day) to the ALD mice, we found that HTF alleviated liver lipid deposition (inhibition of TG, TC, LDL-C) by reducing liver oxidative-stress-mediated inflammation (up-regulation NRF2/HO-1 and down-regulation TLR4/MyD88/NF-κB pathway) and reshaping the gut microbiota (Lactobacillus, Bifidobacterium, Bacillus increased). Overall, we found HTF could be a potential protective natural compound for treating ALD via the gut-liver axis and guaijaverin might be the key substance involved.

Pu-erh tea increases the metabolite Cinnabarinic acid to improve circadian rhythm disorder-induced obesity.

Obesity is one of the circadian rhythm disorders (CRD)-mediated metabolic disorder syndromes. Pu-erh tea is a viable dietary intervention for CRD, however its effect on CRD-induced obesity is unclear. Here, we found that Pu-erh tea improved obesity in CRD-induced mice, which stemmed from the production of Cinnabarinic acid (CA). CA promoted adipose tissue lipolysis and thermogenic response (HSL, ATGL, Pparα, CKB, UCP1) and increased adipocyte sensitivity to hormones and neurotransmitters by targeting the expression of adipose tissue receptor proteins (Q6KAT8, P51655, A2AKQ0, M0QWX7, Q6ZQ33, and mGluR4). This improved mitochondrial activity and facilitated adipose tissue metabolic processes, thereby accelerating glucolipid metabolism. Also, CA-induced alterations in gut microbes and short-chain fatty acids further improved CRD-mediated lipid accumulation. These results suggest that the increase of CA caused by Pu-erh tea, targeted to adipose tissue via the metabolite-blood circulation-adipose tissue axis, maybe a key mechanism for reducing the development of CRD-induced obesity.

Luteolin Ameliorates Methamphetamine-Induced Podocyte Pathology by Inhibiting Tau Phosphorylation in Mice.

Methamphetamine (METH) can cause kidney dysfunction. Luteolin is a flavonoid compound that can alleviate kidney dysfunction. We aimed to observe the renal-protective effect of luteolin on METH-induced nephropathies and to clarify the potential mechanism of action. The mice were treated with METH (1.0-20.0 mg/kg/d bodyweight) for 14 consecutive days. Morphological studies, renal function, and podocyte specific proteins were analyzed in the chronic METH model in vivo. Cultured podocytes were used to support the protective effects of luteolin on METH-induced podocyte injury. We observed increased levels of p-Tau and p-GSK3ß and elevated glomerular pathology, renal dysfunction, renal fibrosis, foot process effacement, macrophage infiltration, and podocyte specific protein loss. Inhibition of GSK3ß activation protected METH-induced kidney injury. Furthermore, luteolin could obliterate glomerular pathologies, inhibit podocyte protein loss, and stop p-Tau level increase. Luteolin could also abolish the METH-induced podocyte injury by inactivating GSK3ß-p-Tau in cultured podocytes. These results indicate that luteolin might ameliorate methamphetamine-induced podocyte pathology through GSK3ß-p-Tau axis.

Pu-erh Tea Restored Circadian Rhythm Disruption by Regulating Tryptophan Metabolism.

Pu-erh tea is a healthy beverage rich in phytochemicals, and its effect on the risk of inducing circadian rhythm disorders (CRD) is unclear. In this study, healthy mice were given water or 0.25% (w/v) Pu-erh tea for 7 weeks, followed by a 40 day disruption of the light/dark cycle. CRD caused dysregulation of neurotransmitter secretion and clock gene oscillations, intestinal inflammation, and disruption of intestinal microbes and metabolites. Pu-erh tea boosted the indole and 5-hydroxytryptamine pathways of tryptophan metabolism via the gut-liver-brain axis. Furthermore, its metabolites (e.g., IAA, Indole, 5-HT) enhanced hepatic glycolipid metabolism and down-regulated intestinal oxidative stress by improving the brain hormone release. Tryptophan metabolites and bile acids also promoted liver lipid metabolism and inhibited intestinal inflammation (MyD88/NF-κB) via the enterohepatic circulation. Collectively, 0.25% (w/v) Pu-erh tea has the potential to prevent CRD by promoting indole and 5-HT pathways of tryptophan metabolism and signaling interactions in the gut-liver-brain axis.

Ripened Pu-Erh Tea Improved the Enterohepatic Circulation in a Circadian Rhythm Disorder Mice Model.

Glucolipid metabolism, nitrogen metabolism, and inflammation are closely related to circadian rhythm disorder (CRD). Ripened Pu-erh tea (RPT) shows significant antidyslipidemic, antihyperurecemic, and anti-inflammatory effects. However, it is unclear whether healthy population are affected by CRD and whether long-term consumption of RPT can alleviate it. To investigate this problem, healthy mice were pretreated with RPT (0.25%, w/v) for 60 days and then subjected to CRD for 40 days. Our results indicated that healthy mice showed obesity, and the intestinal and liver inflammation increased after CRD, which were associated with the development of a metabolic disorder syndrome. RPT effectively reversed this trend by increasing the production and excretion rates of bile acid. RPT reshaped the disorder of gut microbiota caused by CRD and promoted the change of archaeal intestinal types from Firmicutes-dominant type to Bacteroidota-dominant type. In addition, by repairing the intestinal barrier function, RPT inhibited the infiltration of harmful microorganisms or metabolites through enterohepatic circulation, thus reducing the risk of chronic liver inflammation. In conclusion, RPT may reduce the risk of CRD-induced obesity in mice by increasing bile acid metabolism. The change of bile acid pool contributes to the reshaping of gut microflora, thus reducing intestinal inflammation and oxidative stress induced by CRD. Therefore, we speculated that the weakening of CRD damage caused by RPT is due to the improvement of bile acid-mediated enterohepatic circulation. It was found that 0.25% RPT (a human equivalent dose of 7 g/60 kg/day) has potential for regulating CRD.

Saponins from Panax japonicus attenuate cognitive impairment in ageing rats through regulating microglial polarisation and autophagy.

CONTEXT: Panax japonicus is the dried rhizome of Panax japonicus C.A. Mey. (Araliaceae). Saponins from Panax japonicus (SPJ) exhibit anti-inflammatory and antioxidative effects. OBJECTIVE: To explore the neuroprotective effect of SPJ on natural ageing of rat. MATERIALS AND METHODS: Sprague-Dawley (SD) rats 18-month-old were divided into ageing control, ageing treated with SPJ 10 or 30 mg/kg (n = 8). Five-month-old rats were taken as the adult control (n = 8). Rats were fed regular feed or feed containing SPJ for 4 months. Cognitive level was evaluated by Morris water maze (MWM) test. The mechanisms of SPJ's neuroprotection were evaluated by transmission electron microscope, western blot analysis, and immunofluorescence in vivo and in vitro. RESULTS: SPJ attenuated ageing-induced cognitive impairment as indicated by elevated number of times crossing the target platform (from 1.63 to 3.5) and longer time spent in the target platform quadrant (from 1.33 to 1.98). Meanwhile, SPJ improved the morphology of microglia and synapse, and activated M2 microglia polarisation including increased hippocampus levels of CD206 (from 0.98 to 1.47) and YM-1 (from 0.67 to 1.1), and enhanced autophagy-related proteins LC3B (from 0.48 to 0.82), Beclin1 (from 0.32 to 0.51), Atg5 (from 0.22 to 0.89) whereas decreased p62 level (from 0.71 to 0.45) of ageing rats. In vitro study also showed that SPJ regulated the microglial polarisation and autophagy. DISCUSSION AND CONCLUSIONS: SPJ improved cognitive deficits of ageing rats through attenuating microglial inflammation and enhancing microglial autophagy, which could be used to treat neurodegenerative disorders.

Aged Ripe Pu-erh Tea Reduced Oxidative Stress-Mediated Inflammation in Dextran Sulfate Sodium-Induced Colitis Mice by Regulating Intestinal Microbes.

Ripened pu-erh tea has the biological activity of antioxidation and anti-inflammation, which inhibits the related parameters of colitis. However, the role of storage-induced changes in bioactive ingredients of ripened pu-erh tea in colitis remains unclear. In this study, 3.5% dextran sulfate sodium-induced colitis mice were treated with 10 mg/kg bw/day extracts, aged 14 years (P2006) and unaged (P2020) ripened pu-erh tea, respectively, for 1 week. We found that ripened pu-erh tea, especially P2006, inhibited the intestinal oxidative stress-mediated inflammation pathway (TLR4/MyD88/ROS/p38MAPK/NF-κB p65), upregulated the expression of intestinal tight junction proteins (Mucin-2, ZO-1, occludin), promoted M2 polarization of macrophages, and in turn, improved the intestinal immune barrier, which stemmed from the reshaping of intestinal microbiota (e.g., increased Lachnospiraceae_NK4A136_group and Akkermansia levels). Our results speculate that drinking aged ripe pu-erh tea (10 mg/kg bw/day in mice, a human equivalent dose of 7 g/60 kg bw/day) has a practical effect on alleviating and preventing the development of intestinal inflammation.

Performance of sludge drying reed beds for the leachate purification: Effects of sludge loading frequencies and plant species.

Sludge drying reed beds (SDRBs), as a natural biological technology, have positive effects on surplus sludge treatment. However, few studies focus on the sludge leachate purification in the SDRBs regarding the wetland plant species and sludge loading rates. In this study, four SDRBs planted with two wetland plant species (Phragmites australis, Typha angustifolia) were investigated for leachate purification under six sludge loading volumes and feeding frequencies (9L/3d, 6L/3d, 4L/d, 3L/d, 2.5L/d, and 2L/d). Results showed that the lowest Escherichia coli content of 630 number/mL was determined in the P. australis SDRBs, with 86.2-92.8% lower than those in the T. angustifolia controls. However, similar removal efficiencies of chemical oxygen demand (COD), total nitrogen (TN), ammonium (NH4+), total phosphorus (TP), and heavy metals were obtained in the SDRBs with both plant species. Moreover, the optimum sludge loading volume and feeding frequency of 3L/d was determined in the P. australis system, with pollutants (COD, TN, NH4+, and TP) mass removal efficiencies in the leachate being over 94.9%. In addition, the principal component analysis indicated that water loss and oxidation-reduction potential had positive influences on pollutant removal in the planted SDRBs. Overall, the best leachate removal efficiency was obtained in the P. australis SDRBs under the sludge loading volume and feeding frequency of 3L/d.

Thalidomide-induced serious RR interval prolongation (longest interval >5.0 s) in multiple myeloma patient with rectal cancer: A case report.

Primary secondary tumor increased recently with the use of immunomodulatory drugs in patients with multiple myeloma (MM). However, MM with prior diagnosis of primary secondary tumor is relatively rare. In this study, we reported an MM patient with prior diagnosis of rectal cancer. In brief, an 85-year-old man was first diagnosed with rectal cancer. Given the age, heart failure and small-cell hypochromic anemia (hemoglobin level: 54 g/L), rectal cancer resection was not advised and symptomatic treatments were performed (including sufficient iron supplementation). Eight months later, the patient was diagnosed with MM due to worsening anemia. Anemia and heart failure were corrected after three cycles of treatment with thalidomide, dexamethasone and capecitabine. Radical resection of rectal carcinoma (Hartmann) was finally performed due to acute abdominal distension. Meanwhile, RR interval prolongation (longest interval >5.0 s) and atrial fibrillation occurred in the fifth cycle treatment. One month after discontinuation of thalidomide, RR interval returned to normal range, while atrial fibrillation developed into persistent atrial fibrillation.