Loss of microbial functional diversity following Spartina alterniflora invasion reduces the potential of carbon sequestration and nitrogen removal in mangrove sediments-from a gene perspective.

Mangrove ecosystems play an important role in carbon (C) sequestration and nitrogen (N) removal. Although Spartina alterniflora has successively invaded native mangrove habitats during the preceding two decades, the effects of this invasion on the microbial functional potential involved in nutrient cycling remain unclear. In this study, metagenomic sequencing was used to investigate microbial C and N cycling in sediments derived from S. alterniflora and three native mangrove species (Kandelia obovata, Avicennia marina, and Aegiceras corniculatum). Greater differences in functional profiles of C and N cycling-related genes were observed between S. alterniflora and mangrove sediments than between different mangrove sediments. Functional diversity was lower in S. alterniflora sediments than in native mangrove sediments. The growth of Thaumarchaeota and Proteobacteria, was enhanced due to their resilience to diversity loss, while the growth of oligotrophs, such as Chloroflexi and Firmicutes, was inhibited in S. alterniflora sediments. Compared to mangrove sediments, the abundance of genes involved in C fixation and methane production was lower in S. alterniflora sediments. However, S. alterniflora significantly increased the gene abundance of pmo which controlled the oxidation process of CH4 to carbon dioxide. Additionally, genes involved in nitrification were enriched, whereas genes involved in N reduction processes, such as denitrification and dissimilatory nitrate reduction to ammonium, N immobilization, and N mineralization, were depleted in S. alterniflora sediments compared to mangrove sediments. Partial least squares regression models demonstrated that the decrease in soil organic C and increase in pH after S. alterniflora invasion induced the loss of microbial functional diversity, which was the main driver of changes in the abundances of genes involved in C and N cycling. Overall, our findings indicate that S. alterniflora invasion modifies the microbial functional profile of nutrient cycling in native mangrove ecosystems and potentially weakens the capacity of mangroves to sequester carbon and remove nitrogen.

Danggui-Buxue decoction alleviated vascular senescence in mice exposed to chronic intermittent hypoxia through activating the Nrf2/HO-1 pathway.

CONTEXT: As a major risk factor for cardiovascular diseases (CVD), Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH). Recent studies indicated that the increased cardiovascular risk in patients with OSA may be mediated by accelerated vascular senescence. Danggui-Buxue decoction (DBD) has been used for treating cardiovascular diseases, but its mechanism of vascular senescence regulation is still unclear. OBJECTIVE: To investigate the effect of DBD on vascular senescence in mice exposed to CIH and to explore the role of the Nrf2/HO-1 pathway. MATERIALS AND METHODS: C57BL/6N mice were randomly divided into Normoxia control group (CON), CIH (21%-5% O2, 20 times/h, 8 h/d) exposed group (CIH), and DBD treatment group (intragastrically treated with 2.34, 4.68, or 9.36 g/kg/day of DBD separately for 12 weeks as DBL, DBM, or DBH). Blood pressure, cardiac and vascular function, vascular senescence, inflammation response, oxidative stress, and Nrf2/HO-1 expression were determined. RESULTS: DBD (4.68 and 9.36 g/kg) significantly decreased Tail-cuff blood pressure, increased left ventricular systolic function, and alleviated arterial stiffness and vasorelaxation dysfunction in mice exposed to CIH. DBD treatment reduced SA-ß-gal activity, decreased p16 (0.68-fold, 0.62-fold), P21 (0.58-fold, 0.52-fold), and p53 expressions (0.67-fold, 0.65-fold), and increased SIRT1 expression (2.22-fold, 2.98-fold) in the aortic. DBD treatment decreased IL-6, NF-κB, and TNF-α expressions, decreased MDA but increased SOD levels, and increased Nrf2 (1.8-fold, 1.89-fold) and HO-1 (2.25-fold, 2.43-fold) expression. DISCUSSION AND CONCLUSIONS: DBD could attenuate vascular senescence accelerated by CIH exposure through inhibiting inflammatory response and oxidative stress by activating the Nrf2/HO-1 pathway.

[Effects of intermittent hypoxia stimulation with different frequencies on HT22 cell viability and expression of Hif-1α and p-NF-κB].

Intermittent hypoxia (IH) could induce cognitive impairment through oxidative stress and inflammation. However, the degree of cell damage is closely related to the IH stimulus frequency. IH stimulation with different frequencies also induces opposite results on neuronal cell lines. Therefore, this study was aimed to compare the effects of IH stimulation with three different frequencies on murine hippocampal neuronal HT22 cell activity, and to explore the molecular mechanism of the IH stimulus frequency-related neuron injury. HT22 cells were cultured and divided into control group and three IH stimulation groups with different frequencies. Oxygen concentration in the chamber was circulated between 21% and 1% (IH1 group, 6 cycles/h; IH2 group, 2 cycles/h; IH3 group, 0.6 cycle/h). Cell morphology was observed at 6, 12, 24 and 48 h of IH treatment. Cell viability was determined by the CCK-8 kit, lactate dehydrogenase (LDH) content in cell supernatant was determined by LDH kit, oxidative stress level was detected by the reactive oxygen species (ROS) probe, and protein expression levels of hypoxia inducible factor-1α (Hif-1α) and phosphorylated nuclear factor κB (p-NF-κB) were detected by Western blot. The results showed that, compared with control group, cell number and activity in the three IH groups were decreased, LDH content and ROS levels were increased with the prolongation of IH stimulation time, and the changes were most obvious in the IH1 group among those of the three IH groups. Hif-1α expression and the p-NF-κB/NF-κB ratio were also up-regulated with the prolongation of IH stimulation time, and the changes of IH1 group were the most significant. These results suggest that IH stimulation induces oxidative stress injury in HT22 cells, which is related to increased Hif-1α expression and NF-κB phosphorylation. Moreover, the higher frequency of IH stimulation induces more serious cell injury.

Hydrogen gas reduces chronic intermittent hypoxia-induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation.

Molecular hydrogen is reported to be used medically to ameliorate various systemic pathological conditions. This study aimed to investigate the effect of hydrogen (H2 ) gas on hypertension induced by intermittent hypoxia in rats. The adult rats were exposed to chronic intermittent hypoxia (CIH) 8 hours/day for 5 weeks and/or H 2 gas 2 hours/day. We found that the systolic and diastolic blood pressure (BP) increased significantly in rats exposed to intermittent hypoxia, both of which were markedly attenuated after H treatment. Furthermore, intermittent hypoxia exposure elevated renal sympathetic nerve activity, consistent with plasma norepinephrine. Additionally, H 2 gas significantly improved CIH-induced abnormal vascular relaxation. Nevertheless, inhalation of H 2 gas alone did not cause such changes. Moreover, H 2 gas-treated rats exposed to CIH showed a significant reduction in 8-hydroxy-2 deoxyguanosine content and increases in superoxide dismutase activity, indicating improved oxidative stress. Taken together, these results indicate that H 2 gas has significant effects on the reduction of BP without any side effects. Mechanistically, inhibition of sympathetic activity and reduction of systemic vascular resistance may participate in this process via the antioxidant activity of H 2 .

Effects of triptolide on pharmacokinetics of fenofibrate in rats and its potential mechanism.

Triptolide and fenofibrate are often used together for the treatment of nephrotic syndrome in Chinese clinics. This study investigates the effects of triptolide on the pharmacokinetics of fenofibrate in rats and it potential mechanism. The pharmacokinetics of fenofibrate (20 mg/kg) with or without triptolide pretreatment (2 mg/kg/day for seven days) were investigated. Additionally, the inhibitory effects of triptolide on the metabolic stability of fenofibrate were investigated using rat liver microsome incubation systems. The results indicated that the Cmax (35.34 ± 7.52 vs. 30.43 ± 6.45 µg/mL), t1/2 (6.17 ± 1.15 vs. 4.90 ± 0.82 h) and AUC(0-t) (468.12 ± 35.84 vs. 416.35 ± 32.68 mg h L-1) of fenofibric acid decreased significantly (p < .05). The Tmax of fenofibric acid increased significantly (p < .05) from 5.12 ± 0.36 to 6.07 ± 0.68 h. Additionally, the metabolic stability of fenofibrate was prolonged from 35.8 ± 6.2 to 48.6 ± 7.5 min (p < .05) with the pretreatment of triptolide. In conclusion, these results indicated that triptolide could affect the pharmacokinetics of fenofibric acid, possibly by inhibiting the metabolism of fenofibrate in rat liver when they were co-administered.

Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload.

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl's stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

[The role of adventitia in hypoxic vascular remodeling].

As an important site for the production, storage and release of key regulators for vascular function, the vascular adventitia is thought to be a damage sensing tissue in the vascular wall under certain conditions. The adventitial cells are usually the first ones to respond to vascular stress or injury, and consequently affect the structure and function of blood vessel wall. Growing lines of evidence have shown that the vascular adventitia exhibits the earliest and most prominent changes in vascular remodeling due to hypoxia and related pulmonary hypertension and atherosclerosis. In particular, fibroblasts play an important role in the adaptation and regulation to local microenvironmental changes. This review focuses on the role of vascular adventitia in hypoxia-induced vascular remodeling and the underlying molecular mechanisms.

[Bosentan ameliorates hypertension in rats exposed to chronic intermittent hypoxia through inhibiting renal sympathetic nerve activity].

The purpose of this study is to investigate the effect of the oral endothelin antagonist Bosentan on blood pressure and renal sympathetic nerve activity (RSNA) in rats exposed to chronic intermittent hypoxia (CIH), and to explore the sympathoexcitation mechanism of endothelin-1 (ET-1) in CIH-induced hypertension. Twenty-four male SD rats were randomly divided into normoxia, CIH and Bosentan groups. Rats in the normoxia group were exposed to normoxic environment, and rats in CIH or Bosentan group were exposed to intermittent hypoxia for 3 weeks. Bosentan was given at 50 mg/kg by intragastric administration before intermittent hypoxia exposure in Bosentan group. Systolic blood pressure (SBP) was measured by BP-2000, and the change of RSNA to sodium nitroprusside (SNP) or phenylephrine (PE) was recorded by PowerLab signal acquisition system. Serums of all rats were collected and the contents of ET-1 and norepinephrine (NE) were measured by ELISA. Results showed that blood pressure was gradually increased following CIH exposure compared with the normoxia group during the 3 weeks (P < 0.01, P < 0.01, P < 0.001). The basal RSNA was increased and baroreflex sensitivity was decreased in rats exposed to CIH. Furthermore, the blood pressure was positively correlated with the level of ET-1 in serum in rats exposed to CIH (r = 0.833, P = 0.01). Bosentan administration significantly decreased SBP and basal RSNA, increased the baroreflex sensitivity, and decreased serum NE level in rats exposed to CIH. These results suggest that ET-1 is related with blood pressure elevation in rats exposed to CIH, and Bosentan reverses CIH-induced hypertension by decreasing RSNA.

The mitochondrial genome of Huaaristarchorum (Heude, 1889) (Gastropoda, Cerithioidea, Semisulcospiridae) and its phylogenetic implications.

Research on complete mitochondrial genomes can help in understanding the molecular evolution and phylogenetic relationships of various species. In this study, the complete mitogenome of Huaaristarchorum was characterized to supplement the limited mitogenomic information on the genus Hua. Three distinct assembly methods, GetOrganelle, NovoPlasty and SPAdes, were used to ensure reliable assembly. The 15,691 bp mitogenome contains 37 genes and an AT-rich region. Notably, the cytochrome c oxidase subunit I (COX1) gene, commonly used for species identification, appears to be slow-evolving and less variable, which may suggest the inclusion of rapidly evolving genes (NADH dehydrogenase subunit 6 [ND6] or NADH dehydrogenase subunit 2 [ND2]) as markers in diagnostic, detection, and population genetic studies of Cerithioidea. Moreover, we identified the unreliability of annotations (e.g., the absence of annotations for NADH dehydrogenase subunit 4L [ND4L] in NC_037771) and potential misidentifications (NC_023364) in public databases, which indicate that data from public databases should be manually curated in future research. Phylogenetic analyses of Cerithioidea based on different datasets generated identical trees using maximum likelihood and Bayesian inference methods. The results confirm that Semisulcospiridae is closely related to Pleuroceridae. The sequences of Semisulcospiridae clustered into three clades, of which H.aristarchorum is one; H.aristarchorum is sister to the other two clades. The findings of this study will contribute to a better understanding of the characteristics of the H.aristarchorum mitogenome and the phylogenetic relationships of Semisulcospiridae. The inclusion of further mitochondrial genome sequences will improve knowledge of the phylogeny and origin of Cerithioidea.

Wastewater treatment plant effluents increase the global warming potential in a subtropical urbanized river.

Rivers play a pivotal role in global carbon (C) and nitrogen (N) biogeochemical cycles. Urbanized rivers are significant hotspots of greenhouse gases (GHGs, N2O, CO2 and CH4) emissions. This study examined the GHGs distributions in the Guanxun River, an effluents-receiving subtropical urbanized river, as well as the key environmental factors and processes affecting the pattern and emission characteristics of GHGs. Dissolved N2O, CO2, and CH4 concentrations reached 228.0 nmol L-1, 0.44 mmol L-1, and 5.2 µmol L-1 during the wet period, and 929.8 nmol L-1, 0.7 mmol L-1, and 4.6 µmol L-1 during the dry period, respectively. Effluents inputs increased C and N loadings, reduced C/N ratios, and promoted further methanogenesis and N2O production dominated by incomplete denitrification after the outfall. Increased urbanization in the far downstream, high hydraulic residence time, low DO and high organic C environment promoted methanogenesis. The strong CH4 oxidation and methanogenic reactions inhibited by the effluents combined to suppress CH4 emissions in downstream near the outfall, and the process also contributed to CO2 production. The carbon fixation downstream from the outfall were inhibited by effluents. Ultimately, it promoted CO2 emissions downstream from the outfall. The continuous C, N, and chlorine inputs maintained the high saturation and production potential of GHGs, and altered microbial community structure and functional genes abundance. Ultimately, the global warming potential downstream increased by 186 % and 84 % during wet and dry periods on the 20-year scale, and increased by 91 % and 49 % during wet and dry periods on the 100-year scale, respectively, compared with upstream from the outfall. In urbanized rivers with sufficient C and N source supply from WWTP effluents, the large effluent equivalently transformed the natural water within the channel into a subsequent "reactor". Furthermore, the IPCC recommended EF5r values appear to underestimate the N2O emission potential of urbanized rivers with high pollution loading that receiving WWTP effluents. The findings of this study might aid the development of effective strategies for mitigating global climate change.

Chronic intermittent hypoxia aggravated diabetic cardiomyopathy through LKB1/AMPK/Nrf2 signaling pathway.

Chronic intermittent hypoxia (CIH) may play an important role in the development of diabetic cardiomyopathy (DCM). However, the exact mechanism of CIH-induced myocardial injury in DCM remains unclear. In vivo, the db/db mice exposed to CIH were established, and in vitro, the H9C2 cells were exposed to high glucose (HG) combined with intermittent hypoxia (IH). The body weight (BW), fasting blood glucose (FBG) and food intake were measured every two weeks. The glycolipid metabolism was assessed with the oral glucose tolerance test (OGTT) and insulin resistance (IR). Cardiac function was detected by echocardiography. Cardiac pathology was detected by HE staining, Masson staining, and transmission electron microscopy. The level of reactive oxygen species (ROS) in myocardial tissue was detected by dihydroethidium (DHE). The apoptosis was detected by TUNEL staining. The cell viability, ROS, and the mitochondrial membrane potential were detected by the cell counting kit-8 (CCK-8) assay and related kits. Western blotting was used to analyze the liver kinase B1/AMP-activated protein kinase/ nuclear factor-erythroid 2-related factor 2 (LKB1/AMPK/Nrf2) signaling pathway. CIH exposure accelerated glycolipid metabolism disorders and cardiac injury, and increased the level of cardiac oxidative stress and the number of positive apoptotic cells in db/db mice. IH and HG decreased the cell viability and the level of mitochondrial membrane potential, and increased ROS expression in H9C2 cells. These findings indicate that CIH exposure promotes glycolipid metabolism disorders and myocardial apoptosis, aggravating myocardial injury via the LKB1/AMPK/Nrf2 pathway in vitro and in vivo.

Phosphorus starvation response genes and function coupling: A mechanism to regulate phosphorus availability in a subtropical estuary.

Phosphorus (P) plays an important role in regulating primary production in estuarine environments. However, knowledge of the P-functional gene composition of microbial communities and the mechanisms of microbial adaptation to changes in available P in estuaries remain limited. This study coupling 16 s rDNA and metagenomics sequencing was conducted to reveal the relationship between P cycling functional genes, microbial interactions, and P availability in the Jiulong River Estuary. The results showed that the relative abundance of P cycling functions genes was highest in winter, and lowest in summer. Spatially, the total relative abundance of P cycling functions genes was higher in the riverward than that in the seaward. P cycling functional microbial interactions and P cycling gene coupling were strongest in summer and in the seaward. Changes in both temperature and salinity had significant direct and indirect effects on P cycling function, and the influence of salinity on P cycling function was greater than that on the microbial community in the estuary. Salinity had significant direct negative effects on inorganic P-solubilization (IP), organic P-mineralization (OP), and P uptake and transport functions (PT). Whereas, salinity had a significant positive effect on P-starvation response regulation (PR) function. Thus, salinity and microbial communities regulate the soluble reactive phosphate concentrations in estuarine environments by strengthening internal coupling among P cycling functions, promoting PR function, and facilitating PT gene expression. PR is the most important predictors, PR, PT, and PR-PT together explained 38.56 % of the overall soluble reactive phosphorus (SRP) variation. Over 66 % of the explained SRP variations can be predicted by the PR, PT, and PR-PT functional genes. This finding improves the knowledge base of the microbial processes for P cycling and provides a foundation for eutrophication management strategies in the estuary.

Shengmaisan combined with Liuwei Dihuang Decoction alleviates chronic intermittent hypoxia-induced cognitive impairment by activating the EPO/EPOR/JAK2 signaling pathway.

Chronic intermittent hypoxia (CIH), a principal pathophysiological aspect of obstructive sleep apnea (OSA), is associated with cognitive deficits. Clinical evidence suggests that a combination of Shengmaisan and Liuwei Dihuang Decoctions (SMS-LD) can enhance cognitive function by nourishing yin and strengthening the kidneys. This study aimed to assess the efficacy and underlying mechanisms of SMS-LD in addressing cognitive impairments induced by CIH. We exposed C57BL/6N mice to CIH for five weeks (20%-5% O2, 5 min/cycle, 8 h/day) and administered SMS-LD intragastrically (15.0 or 30 g·kg-1·day) 30 min before each CIH session. Additionally, AG490, a JJanus kinase 2 (JAK2) inhibitor, was administered via intracerebroventricular injection. Cognitive function was evaluated using the Morris water maze, while synaptic and mitochondrial structures were examined by transmission electron microscopy. Oxidative stress levels were determined using DHE staining, and the activation of the erythropoietin (ER)/ER receptor (EPOR)/JAK2 signaling pathway was analyzed through immunohistochemistry and Western blotting. To further investigate molecular mechanisms, HT22 cells were treated in vitro with either SMS-LD medicated serum alone or in combination with AG490 and then exposed to CIH for 48 h. Our results indicate that SMS-LD significantly mitigated CIH-induced cognitive impairments in mice. Specifically, SMS-LD treatment enhanced dendritic spine density, ameliorated mitochondrial dysfunction, reduced oxidative stress, and activated the EPO/EPOR/JAK2 signaling pathway. Conversely, AG490 negated SMS-LD's neuroprotective and cognitive improvement effects under CIH conditions. These findings suggest that SMS-LD's beneficial impact on cognitive impairment and synaptic and mitochondrial integrity under CIH conditions may predominantly be attributed to the activation of the EPO/EPOR/JAK2 signaling pathway.

Microplastics strengthen nitrogen retention by intensifying nitrogen limitation in mangrove ecosystem sediments.

Mangrove wetlands are hotspots of the global nitrogen (N) cycle and important sinks of microplastics (MPs) due to their ecotone location between terrestrial and marine ecosystems. However, the effects of MPs on N cycle processes in mangrove ecosystems are still poorly understood. Thus, the present study assessed the impacts by adding MPs to mangrove sediments in a microcosm incubation experiment. The results showed that MPs increased dissolved organic carbon and nitrate but reduced ammonium contents in the sediments. MPs increased C:N stoichiometric and N:C-acquiring enzymatic ratios, indicating an intensified N limitation in mangrove sediments following exposure of MPs. MPs decreased microbial community diversity and shifted sediment microbial communities from r- to K-strategists, consistent with the intensified N limitation. In response, dissimilatory nitrate reduction to ammonium (DNRA) rates increased while nitrous oxide (N2O) production reduced suggesting more efficient N utilization in MPs treatments. The MPs with heteroatoms such as PLA- and PVC-MPs, increased DNRA rates by 67.5-78.7%, exhibiting a stronger impact than PE-MPs. The variation partitioning analysis revealed that the variances of DNRA rates and N2O production could be attributed to synergistic effects of physicochemical properties, nutrient limitation, and microbial community in mangrove sediments. Overall, this study provides pertinent insights into the impacts of MPs as a new carbon source on nutrient limitation and N turnover in mangrove ecosystems.

Land use/cover drive functional patterns of bacterial communities in sediments of a subtropical river, China.

The bacterial community in sediment serves as an important indicator for assessing the environmental health of river ecosystems. However, the response of bacterial community structure and function in river basin sediment to different land use/cover changes has not been widely studied. To characterize changes in the structure, composition, and function of bacterial communities under different types of land use/cover, we studied the bacterial communities and physicochemical properties of the surface sediments of rivers. Surface sediment in cropland and built-up areas was moderately polluted with cadmium and had high nitrogen and phosphorus levels, which disrupted the stability of bacterial communities. Significant differences in the α-diversity of bacterial communities were observed among different types of land use/cover. Bacterial α-diversity and energy sources were greater in woodlands than in cropland and built-up areas. The functional patterns of bacterial communities were shown that phosphorus levels and abundances of pathogenic bacteria and parasites were higher in cropland than in the other land use/cover types; Urban activities have resulted in the loss of the denitrification function and the accumulation of nitrogen in built-up areas, and bacteria in forested and agricultural areas play an important role in nitrogen degradation. Differences in heavy metal and nutrient inputs driven by land use/cover result in variation in the composition, structure, and function of bacterial communities.

Soil organic carbon storages and bacterial communities along a restored mangrove soil chronosequence in the Jiulong River Estuary: From tidal flats to mangrove afforestation.

Among many ecological services provided by mangrove ecosystems, soil organic carbon (SOC) storages have recently received much attention owing to the increasing atmospheric partial pressure of dissolved CO2 (pCO2). Bacteria are fundamental to ecosystem functions and strongly influence the coupling of coastal carbon, nitrogen, and sulfur cycling in soils. The SOC storage and bacterial communities along a restored mangrove soil chronosequence in the Jiulong River Estuary were explored using the 16S rDNA sequencing technique. The results showed the SOC storage in the 100 cm soil profile was 103.31 ± 5.87 kg C m-2 and 93.10 ± 11.28 kg C m-2 for mangroves with afforestation ages of 36 and 60 years, respectively. The total nitrogen (TN) and total sulfur (TS) contents exhibited significant correlations with the SOC in the mangrove soils, but only TN and SOC showed significant correlation in tidal flat soils. Although the tidal flats and mangroves occupied the contiguous intertidal zone within several kilometers, the variations in the SOC storage along the restored mangrove soil chronosequence were notably higher. The Functional Annotation of Prokaryotic Taxa (FAPROTAX) database was used to annotate the metabolic functions of the bacteria in the soils. The annotation revealed that only four metabolic functions were enriched with a higher relative abundance of the corresponding bacteria, and these enriched functions were largely associated with sulfate reduction. In addition, the specifically critical bacterial taxa that were associated with the SOC accumulation and nutrient cycling, shaped the distinct metabolic functions, and consequently facilitated the SOC accumulation in the mangrove soils with various afforestation ages. The general homogenization of the microbial community and composition along the intertidal soil chronosequence was primarily driven by the reciprocating tidal flows and geographical contiguity.

Tanshinone IIA inhibited intermittent hypoxia induced neuronal injury through promoting autophagy via AMPK-mTOR signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Chronic intermittent hypoxia (CIH) is the primary pathophysiological process of obstructive sleep apnea (OSA) and is closely linked to neurocognitive dysfunction. Tanshinone IIA (Tan IIA) is extracted from Salvia miltiorrhiza Bunge and used in Traditional Chinese Medicine (TCM) to improve cognitive impairment. Studies have shown that Tan IIA has anti-inflammatory, anti-oxidant, and anti-apoptotic properties and provides protection in intermittent hypoxia (IH) conditions. However, the specific mechanism is still unclear. AIM OF THE STUDY: To assess the protective effect and mechanism of Tan IIA treatment on neuronal injury in HT22 cells exposed to IH. MATERIALS AND METHODS: The study established an HT22 cell model exposed to IH (0.1% O2 3 min/21% O2 7 min for six cycles/h). Cell viability was determined using the Cell Counting Kit-8, and cell injury was determined using the LDH release assay. Mitochondrial damage and cell apoptosis were observed using the Mitochondrial Membrane Potential and Apoptosis Detection Kit. Oxidative stress was assessed using DCFH-DA staining and flow cytometry. The level of autophagy was assessed using the Cell Autophagy Staining Test Kit and transmission electron microscopy (TEM). Western blot was used to detect the expressions of the AMPK-mTOR pathway, LC3, P62, Beclin-1, Nrf2, HO-1, SOD2, NOX2, Bcl-2/Bax, and caspase-3. RESULTS: The study showed that Tan IIA significantly improved HT22 cell viability under IH conditions. Tan IIA treatment improved mitochondrial membrane potential, decreased cell apoptosis, inhibited oxidative stress, and increased autophagy levels in HT22 cells under IH conditions. Furthermore, Tan IIA increased AMPK phosphorylation and LC3II/I, Beclin-1, Nrf2, HO-1, SOD2, and Bcl-2/Bax expressions, while decreasing mTOR phosphorylation and NOX2 and cleaved caspase-3/caspase-3 expressions. CONCLUSION: The study suggested that Tan IIA significantly ameliorated neuronal injury in HT22 cells exposed to IH. The neuroprotective mechanism of Tan IIA may mainly be related to inhibiting oxidative stress and neuronal apoptosis by activating the AMPK/mTOR autophagy pathway under IH conditions.

Growth and physiological response of Kandelia obovata and Bruguiera sexangula seedlings to aluminum stress.

The role of mangroves as a biogeochemical buffer for heavy metal pollutants in coastal wetlands has been demonstrated, but knowledge gaps still exist on the tolerant capacity of mangroves to aluminum (Al). This study assessed the growth and physiological response of viviparous mangroves Kandelia obovata and Bruguiera sexangula to Al stress. The two mangrove seedlings were treated with AlCl3 at concentrations of 0 (as control) to 100 mmol L-1, and the impact of Al on their growth and antioxidant parameters were determined. Additionally, the accumulation and translocation of metal elements were estimated in B. sexangula seedlings under relative long-term Al stress. K. obovata appeared to survive with a tolerance potential of 10 mmol L-1 AlCl3, whereas B. sexangula had a higher tolerant ability of 50 mmol L-1 AlCl3. Both root elongation and seedling growth were inhibited by Al stress. The exposure to 25-100 mmol L-1 AlCl3 induced increases in membrane lipid peroxidation and osmoprotectant molecule (proline) in mangrove seedlings. Both mangrove seedlings revealed significant changes in antioxidant enzyme activities that were attributed to Al stress-induced oxidative damages. The activities of superoxide dismutase, catalase, peroxidase, and/or ascorbate peroxidase were differently impacted by the treatment time (7 days for short term versus 60 days for long term) and AlCl3 concentrations in K. obovata and B. sexangula seedlings. For B. sexangula seedlings, Al accumulation was in an order root > leaf > stem, whereas the translocation of metal elements in the aboveground tissues (leaf and stem) was differently impacted by Al stress. In conclusion, this study provides insights into different Al-tolerant abilities operated in two mangrove species that are widespread in coastal wetlands of China.

Shashen-Maidong Decoction inhibited cancer growth under intermittent hypoxia conditions by suppressing oxidative stress and inflammation.

ETHNOPHARMACOLOGICAL RELEVANCE: Lung cancer is one of the most common malignant tumours and has become the leading cause of cancer-related deaths worldwide. Abnormal microcirculation during tumour growth leads to intermittent hypoxia (IH), which is responsible for promoting cancer cell proliferation and migration. Patients with advanced lung cancers show deficiency of both Qi and Yin Syndrome (DQYS) in TCM, and studies have confirmed that IH exposure is related to DQYS. Shashen-Maidong Decoction (SMD), has been widely applied clinically targeting DQYS and has a long history for treating lung cancer by nourishing the body's "zheng qi" and resisting "xie qi". However, whether SMD could be beneficial to lung cancer under IH conditions remains unclear. AIM OF THE STUDY: This study aimed to clarify the effects and mechanism of SMD on non-small cell lung cancer (NSCLC) growth under IH conditions. MATERIALS AND METHODS: C57 mice were injected subcutaneously into the right axilla with Lewis lung cancer (LLC) cells and exposed to IH conditions (21%-5% O2, 5 min/cycle, 8 h/day) for 21 days. SMDs were orally treated with different concentrations (2.6, 5.2 or 10.4 g/kg/day) 30 min before IH exposure. Tumour proliferation and migration were assessed by HE and IHC staining, and oxidative stress was assessed by DHE staining and MDA or SOD detection. IL-6, IL-1ß and TNF-α levels were assessed by IHC staining, and the IL-6/JAK2/STAT3 signalling pathway was detected by western blotting. RESULTS: Our results showed that SMD treatment inhibited tumour growth and liver metastasis in LLC-bearing mice exposed to IH, decreased Ki67, CD31, VEGF, and MMP-2, and increased E-cadherin expression in tumourt tissue. SMD reduced ROS production, increased SOD levels and SOD-2 expression, and decreased MDA levels and NOX-2 expression. SMD decreased IL-6, IL-1ß and TNF-α levels, reduced IL-6 expression and inhibited JAK2 and STAT3 phosphorylation. Additionally, SMD treatment improved DQYS and liver and kidney function in LLC-bearing mice under IH conditions. CONCLUSION: Our research suggests that SMD treatment can inhibit tumour growth in mice exposed to IH. The antitumour effect of SMD may be related to attenuated oxidative stress and inflammation through inactivation of the IL-6/JAK2/STAT3 signalling pathway under IH conditions.

Therapeutic Potential of Astragaloside IV Against Adriamycin-Induced Renal Damage in Rats via Ferroptosis.

Adriamycin (ADR) has been utilized to treat cancer for several decades. However, ADR-induced renal injury is one of the most common side effects accompanying ADR therapy. In the present study, we revealed that astragaloside IV (ASIV) was beneficial for renal injury caused by Adriamycin. We demonstrated that ASIV significantly ameliorated kidney injury, improved renal dysfunction, reduced oxidative stress, alleviated iron accumulation, and inhibited the induction of ferroptosis by ADR. ASIV also rescued the intracellular levels of nuclear factor-erythroid-2-related factor 2 (Nrf2) and promoted nuclear translocation of Nrf2. These protective effects of ASIV on renal injury might be attained through the ASIV-induced activation of the Pi3K/Akt signaling pathway. In vitro, the treatment of the HK-2 cells with fer-1 or deferoxamine mesylate obviously improved cell viability during Adriamycin administration. On the other hand, the protective role of ASIV can be abrogated by RSL3 to some extent. Moreover, ASIV lowered the expression of transferrin receptor 1 and divalent metal transporter 1 while enhancing the expression of ferropotin 1 and glutathione peroxidase 4 in ADR administrated cells, the effects of which were akin to those of deferoxamine mesylate. Furthermore, ASIV increased the phosphorylation of Pi3K, Akt, and the expression of Nrf2 and glutathione peroxidase 4 compared to HK-2 cells stimulated by ADR. However, Pi3K inhibitor LY294002 abrogated these activations. In conclusion, ferroptosis may involve in ADR-induced nephrotoxicity, and ASIV might protect nephrocytes against ADR-induced ferroptosis, perhaps via activations of the Pi3K/Akt and Nrf2 signaling pathways.