Combined role of ground cover management in altering orchard surface‒subsurface erosion and associated carbon-nitrogen-phosphorus loss.

The combined role of ground cover management in controlling soil erosion and nutrient loss from new orchards is still less understood. In this study, four ground cover management practices, orchard with grass cover (OG), orchard with interplant cover (OI), orchard with straw cover (OS), and orchard with bare ground (OB), were designed to identify their impacts on soil erosion and associated carbon-nitrogen-phosphorus loss in new orchards by rainfall simulation tests with rainfall intensities of 60, 90, and 120 mm h-1 and 90 min rainfall duration. The results showed that OS had the lowest surface flow coefficient (6.6%) and highest subsurface flow coefficient (32.5%). The highest soil loss rate occurred in the OB plot (65.4 g m-2 min-1), and the lowest soil loss rate occurred in the OS plot (0.5 g m-2 min-1). OS plot showed better effectiveness in improving soil erosion. However, the increased infiltration capacity was facilitated in terms of causing non-point source pollution. The C-N-P ratios of surface flow in different cover measures (OB, OI, OG, and OS) were 1.4:1.2:0.9:1, 1.8:1.7:1.2:1, and 2.3:1.9:1.2:1, respectively. The ratios of sediment in different cover measures were 7.3:9:2.3:1, 2:1.5:1.2:1, and 1.2:1:0.8:0.7, respectively. Cover management plots play an active role in reducing nutrient loss in surface flow and sediment, but the increased infiltration in covered management plots is associated with the risk of groundwater contamination in subsurface flow. The C-N-P ratios of subsurface flow in OB and covered managed plots (OI, OG, and OS) were 1:3.3:1.6:2.7, 1:1.5:2.2:2.4 and 1:1.2:1.5:1.3, respectively. Therefore, when managing the phenomenon of soil erosion through ground cover measures, attention should also be focused on the function of cover measures in regulating non-point source pollution underground, such as subsurface flow. This research recommends a combination of cover management measures to further mitigate erosion and the risk of groundwater contamination.

Pseudognaphalium affine Extract Alleviates COPD by Inhibiting the Inflammatory Response via Downregulation of NF-κB.

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with limited therapeutic options. Pseudognaphalium affine (D. Don) Anderb. is a medicinal and edible plant used to treat cough, asthma, and COPD for a long time in folk medicine. The objective of this study is to evaluate the effect of Pseudognaphalium affine (D. Don) Anderb. extract (GAE) and investigate the possible underlying mechanism in vivo and in vitro. In vivo, the administration of GAE in a rat COPD model could significantly ameliorate lung damage and pulmonary function by inhibiting the production of pro-inflammatory cytokines. Western blot and real-time PCR results showed that GAE could suppress nuclear translocation of nuclear factor-kappa B (NF-κB), which indicated that GAE down-regulated the NF-κB pathway. Moreover, GAE protected against tumor necrosis factor (TNF)-α induced inflammatory response in BEAS-2B and inhibited the NF-κB pathway. All data suggested that GAE exhibited its anti-COPD effect by inhibiting pro-inflammatory cytokines, which may be associated with the inhibition of the NF-κB pathway.

Polydatin alleviates DSS- and TNBS-induced colitis by suppressing Th17 cell differentiation via directly inhibiting STAT3.

Inflammatory bowel disease (IBD) is a non-specific chronic intestinal inflammatory disease, often presenting with abdominal pain, diarrhea, bloody stool, anorexia, and body loss. It is difficult to cure completely and a promising treatment is urgently needed. Natural compounds can offer promising chemical agents for treatment of diseases. Polydatin is a natural ingredient extracted from the dried rhizome of Polygonum cuspidatum, which has anti-inflammatory, anti-tumor, and dementia protection activities. The purpose of this study was to evaluate the therapeutic effect of polydatin on IBD and explore its possible mechanism. We found that polydatin could effectively suppress the differentiation of Th17 cells in vitro, but had no effect on the differentiation of Treg cells. Polydatin significantly alleviated colitis induced by dextran sulfate sodium (DSS) and 2, 4, 6-trinitrobenzenesulfonic acid (TNBS) in mice, and dramatically decreased the proportion of Th17 cells in spleen and mesenteric lymph nodes. Mechanism investigations revealed that polydatin specifically inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation by directly binding to STAT3, leading to Th17 cell reduction and thereby alleviating colitis. These findings provide novel insights into the anti-colitis effect of polydatin, which may be a promising drug candidate for the treatment of IBD.

Neobaicalein Inhibits Th17 Cell Differentiation Resulting in Recovery of Th17/Treg Ratio through Blocking STAT3 Signaling Activation.

Huangqin is the dried root of Scutellaria baicalensis Georgi, which has been widely utilized for heat-clearing (Qingre) and dewetting (Zaoshi), heat-killed (Xiehuo) and detoxifying (Jiedu) in the concept of Traditional Chinese Medicine and is used for treating inflammation and cancer in clinical formulas. Neobaicalein (NEO) is of flavonoid isolated from Huangqin and has been reported to possess prominent anti-inflammatory effects in published work. Th17/Treg balance shift to Th17 cells is an essential reason for autoimmune inflammatory diseases. However, the role NEO plays in Th17 and Treg and the underlying mechanism has not been elucidated yet. Network pharmacology-based study revealed that NEO predominantly regulated IL-17 signaling pathway. Moreover, our result shown that NEO (3-30 µmol/L) down-regulated Th17 differentiation and cellular supernatant and intracellular IL-17A level and tumor necrosis factor α production in a concentration-dependent manner. The further mechanism research revealed that NEO also specifically inhibited phosphorylation of STAT3(Tyr725) and STAT4 (Y693) without influence on activation of STAT5 and STAT6 in splenocytes. Immunofluorescence results illuminated that NEO effectively blocked STAT3 translocated into nucleus. Interestingly, NEO at appreciated dose could only inhibit Th17 cell differentiation and have no effect on Treg differentiation. The present study revealed that NEO effectively inhibited Th17 cell differentiation through specifically blocking the activation of STAT3 signaling without inactivation of STAT5 and STAT6. Additional inhibitory effect on activation of STAT4 by NEO also suggested the potential for antagonism against Th1 differentiation. All work suggested that NEO may be a potential candidate for immunoregulation and treating autoimmune inflammatory diseases through inhibiting immune cell viability and T cell differentiation.

Gualou Guizhi Granule Suppresses LPS-Induced Inflammatory Response of Microglia and Protects against Microglia-Mediated Neurotoxicity in HT-22 via Akt/NF-κB Signaling Pathways.

Neuroinflammation plays a crucial part in the commencement and advancement of ischemic stroke. Gualou Guizhi granule (GLGZG) is known to well exhibit neuroprotective effect, but it is not known whether GLGZG can regulate the inflammatory process at the cellular level in BV2 microglia cells and protect against microglia-mediated neurotoxicity in neurons. Herein, we aimed to investigate the anti-inflammatory effects of GLGZG on BV2 microglia cells and protection against microglia-mediated neurotoxicity in neurons. Methods. The cell model of neuroinflammation was constructed by lipopolysaccharide (LPS) to observe the effect of GLGZG in the presence or absence of GLGZG. The production of nitric oxide (NO), inflammatory mediators, was detected. Moreover, potential mechanisms associated with the anti-inflammatory effect, such as inhibition of microglial activation and nuclear factor kappa B (NF-κB), were also investigated. In addition, to prove whether GLGZG protects against microglia-mediated neurotoxicity, neuronal HT-22 cells were cultured in the conditioned medium. And cell survivability and neuronal apoptosis of HT-22 were evaluated. Results. It was found that a main regulator of inflammation, NO, is suppressed by GLGZG in BV2 microglial cells. Moreover, GLGZG dose dependently decreased the mRNA and protein levels of inducible NO synthase (iNOS) in LPS-stimulated BV2 cells. Additionally, GLGZG inhibited the expression and secretion of proinflammatory cytokines in BV2 microglial cells. Also, GLGZG inhibited LPS-activated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in BV2 microglial cells at the intracellular level. GLGZG significantly affected Akt phosphorylation: phosphorylated forms of Akt increased. To check whether GLGZG protects against microglia-mediated neurotoxicity, neuronal HT-22 cells were incubated in the conditioned medium. GLGZG showed a neuroprotective effect by promoting cell survivability and suppressing neuronal apoptosis. Conclusions. GLGZG exerted its potential effects on suppressing inflammatory responses in LPS-induced BV2 cells by regulating NF-κB and Akt pathways. In addition, GLGZG could protect against microglia-mediated neurotoxicity in HT-22.

Vitamin K alleviates bone calcium loss caused by Salmonella Enteritidis through carboxylation of osteocalcin.

BACKGROUND: The present study aimed at evaluating the effect of vitamin K (VK) supplementation on bone health of laying hens challenged by Salmonella Enteritidis. METHODS: A total of 80 32-week-old double negative salmonella-free brown-egg laying hens were randomly assigned to 4 treatments with 20 replicates each (1 bird per replicate) according to a 2 × 2 factorial design with 2 dietary VK supplementation levels [0 mg/kg (VK0) vs 2 mg/kg VK (VK2) and 2 challenge treatments [Salmonella Enteritidis (SE) vs physiological saline solution (PS)]. During the last 3 days of week 43 of age, birds of both VK treatments were either orally challenged with 1.0 mL suspension of 109 cfu/mL S. Enteritidis daily or received the same volume of PS. RESULTS: The laying rate, daily egg mass, tibia strength, CT, cOC and cOC/(cOC + ucOC) of VK2 treatment increased (P < 0.05) in contrast to VK0, however, the medullary area and ucOC of VK2 treatment decreased (P < 0.05) in contrast to VK0. Mortality, medullary area, serum Ca content of SE treatments increased (P < 0.05) in contrast to PS treatments. In both SE treatments, the decrease (P < 0.05) in birds' tibia strength was associated with higher (P < 0.05) Ca levels in serum. There is an interaction (P < 0.05) between SE challenge and VK levels with regard to tibia strength and serum Ca levels. At week 42, serum CT was positively correlated with cOC (R = 0.99, P = 0.009); at week 44, tibia strength was positively correlated with BMD (R = 0.95, P = 0.045), but negatively correlated with medullary area (R = - 0.98, P = 0.018). CONCLUSIONS: VK (2 mg/kg) supplementation to diets of laying hens can enhance bone strength under challenge situations with Salmonella Enteritidis. Medullary area has proven to be a sensitive biomarker for bone calcium loss caused by SE infection.

An In Vitro Verification of the Effects of Paeoniflorin on Lipopolysaccharide-Exposed Microglia.

BACKGROUND: The neuroprotective effects of Paeoniflorin (PF) are well known. Most of the evidence was verified in vivo. We attempted to perform an in vitro verification of the effects of PF in microglia. METHODS: A lipopolysaccharide- (LPS-) exposed microglia model was employed. An enzyme-linked immunosorbent assay was used to measure the levels of cytokines in the culture supernatants. A real-time polymerase chain reaction was performed to measure the mRNA expression of cytokines and M1- and M2-like genes. A western blot analysis was used to examine the expression of proteins associated with the nuclear factor-kappa B (NF-κB) signaling pathway. RESULTS: We found that the administration of PF reversed the inflammatory response induced by LPS. It downregulated proinflammatory cytokines and upregulated anti-inflammatory cytokines. This, in turn, alleviated the oxidative injuries, downregulated the expression of M1-like genes, and upregulated the expression of M2-like genes. PF can also reverse the changes in proteins associated with the NF-κB signaling pathway induced by LPS. CONCLUSIONS: We provided evidence obtained in vitro concerning the neuroprotective effects of PF via suppressing activation of microglia, which might be associated with the NF-κB signaling pathway. These findings contribute to obtaining a deeper understanding of PF, a potential new treatment for brain injuries.