Aims The effect of increasing dietary cation–anion difference (DCAD) on rumen fermentation and ruminal microbial community in dairy cows under heat stress (HS) conditions were evaluated. Methods and Results This study was performed as a two‐period cross‐over design during the summer season, with eight lactating dairy cows randomly distributed to either a control DCAD diet (CON: 33·5 mEq/100 g DM) or high DCAD diet (HDCAD: 50·8 mEq/100 g DM). Throughout the present study, the temperature and humidity index (THI; 80·2 ± 4·29) was generally elevated above the threshold (THI = 72) that is reported to cause HS in lactating dairy cows. Rumen liquid samples were collected on 15 and 21 d during each 21 d‐period. The absolute concentration of ruminal total volatile fatty acid (TVFA) in HDCAD treatment was significantly (P < 0·05) higher than those in the control, whilst the ruminal pH, NH3‐N, and VFA molar percentages were unaffected through increasing DCAD. Furthermore, the copy numbers of the cellulolytic bacteria Ruminococcus albus and Ruminococcus flavefaciens in rumen fluid significantly (P < 0·05) rose along with the increment of DCAD. Although the Alpha diversity indexes and the bacterial microbiota structure were unaffected, increasing DCAD significantly (P < 0·05) enriched the phylum Fibrobacteres and genus Fibrobacter in the microflora of rumen fluid, whilst the genera Flexilinea and Dubosiella were the most differentially abundant taxa in the control. Conclusions Increasing DCAD under HS conditions resulted in a greater concentration of total VFA without affecting rumen bacteria diversity or structure, although the enrichment of some cellulolytic/hemicellulolytic bacteria was observed. Significance and Impact of the Study The present study provides information on the modulation of rumen fermentation and microbial community through the increment of DCAD in Holstein dairy cows under HS conditions.

ABSTRACT. To explore the mechanism whereby stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) jointly mobilize bone marrow stem cells (BMSCs) and promote kidney repair, male Sprague-Dawley rats were randomly assigned into 4 groups. In the treatment control group, rats were administered SCF (200 μg· kg

The aim of this study was to investigate the effects of stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) on bone marrow-derived stem cell (BMSC) mobilization in rat models of renal ischemia/reperfusion (I/R) injury. In addition, the effects of SCF and G-CSF on cellular apoptosis were explored in order to determine the protective mechanism of the two factors against renal I/R injury. A unilateral renal I/R injury model was established for the model and treatment groups. The treatment and treatment control groups were subcutaneously injected with SCF (200 µg/kg/day) and G-CSF (50 µg/kg/day) 24 h after the establishment of the model for five consecutive days. The total number of leukocytes in the peripheral blood and the cellular percentages of cluster of differentiation (CD)34, renal CD34 and apoptotic cells were detected. The total number of leukocytes in the peripheral blood and the percentages of CD34 cells in the treatment and treatment control groups reached maximum levels on the fifth postoperative day and were significantly higher than those in the normal control and model groups. The number of renal CD34 cells in the treatment group was significantly increased compared with that in the treatment control and model groups. The apoptotic indices (AIs) of the model and treatment groups were higher than those of the normal control and treatment control groups. The AI of the model group was significantly higher than that of the treatment group. In conclusion, the combined application of SCF and G-CSF can mobilize sufficient numbers of BMSCs and cause cellular 'homing' to the injured site, thus inhibiting apoptosis and promoting the repair of renal tubular injury.

The aim of this study was to investigate the effects of erythropoietin (EPO) on the impairment of autophagy induced by lipopolysaccharide (LPS) in primary cultured rat glomerular mesangial cells (GMCs). Rat GMCs were isolated and cultured in normal glucose, high-glucose, LPS or LPS + EPO medium. At 24 and 72 h of culture, the cells were examined for expression levels of the autophagy markers LC3 and p62/sequestosome-1 (SQSTM1) using western blot analysis. At 24 h, no significant difference in the expression of LC3 and p62/SQSTM1 was observed among the groups; however, the cells exposed to high-glucose medium for 72 h showed downregulated LC3 expression and upregulated p62/SQSTM1 expression. The cells exposed to LPS (10 ng/ml) for 72 h showed upregulated LC3 expression and upregulated p62/SQSTM1 expression. These changes were reversed in the LPS + EPO group at 72 h. In conclusion, EPO can inhibit LPS-induced autophagy in rat GMCs.

The present trial was performed to reveal the regulatory effects of L-theanine on the levels of lipopolysaccharide (LPS) endotoxin within different biofluids, as well as relevant inflammatory responses of dairy cattle under heat stress conditions. Thirty lactating Chinese Holstein dairy cattle (189 ± 47 days in milk, and 2 ± 1 parities) were allocated in a completely randomized design to each of 3 dietary treatments: the control (CON, 0 g/d per cow L-theanine), the low L-theanine dosage treatment (LL, 16 g/d per cow L-theanine), and the high L-theanine dosage treatment (HL, 32 g/d per cow L-theanine). This trial consisted of 38 d (7 d for adaption and 31 d for data and sample collection), and sample collection for rumen liquid, blood plasma or serum, and milk were conducted on the d 27 and 38, respectively. Dairy cattle were constantly exposed to environmental heat stress during this experiment according to the recorded temperature-humidity index (THI). In the LL treatment, LPS concentration in rumen liquid was higher ( P < 0.05), whilst LPS densities in plasma and milk were lower ( P < 0.05) than those of the CON. Supplementing L-theanine at 2 dosages both significantly lowered ( P < 0.05) the level of interleukin (IL)-1β in the serum. Results of the present study suggested that L-theanine could be a promising additive in reducing the detrimental effects of heat stress on dairy cows, and L-theanine supplementation at 16 g/d per cow is preferred because it reduced the LPS translocation into the peripheral blood and LPS accumulation in the milk, as well as mitigated LPS-induced inflammatory reactions in dairy cows during heat stress. Further studies are necessitated to investigate the underlying mechanisms of L-theanine in LPS alteration and inflammation alleviation.