Glycine Betaine and ß-Aminobutyric Acid Mitigate the Detrimental Effects of Heat Stress on Chinese Cabbage (Brassica rapa L. ssp. pekinensis) Seedlings with Improved Photosynthetic Performance and Antioxidant System.

Heat stress is one of the major abiotic factors that limit the growth, development, and productivity of plants. Both glycine betaine (GB) and ß-aminobutyric acid (BABA) have received considerable attention due to their roles in stimulating tolerance to diverse abiotic stresses. In order to understand how GB and BABA biostimulants alleviate heat stress in a cool-weather Chinese cabbage (Brassica rapa L. ssp. pekinensis) plant, we investigated the GB- and BABA-primed heat-stressed plants in terms of their morpho-physiological and biochemical traits. Priming with GB (15 mM) and BABA (0.2 mM) was conducted at the third leaf stage by applying foliar sprays daily for 5 days before 5 days of heat stress (45 °C in 16 h light/35 °C in 8 h dark) on Chinese cabbage seedlings. The results indicate that GB and BABA significantly increased chlorophyll content, and the parameters of both gas exchange and chlorophyll fluorescence, of Chinese cabbage under heat stress. Compared with the unprimed heat-stressed control, the dry weights of GB- and BABA-primed plants were significantly increased by 36.36% and 45.45%, respectively. GB and BABA priming also greatly mitigated membrane damage, as indicated by the reduction in malondialdehyde (MDA) and electrolyte leakage through the elevation of proline content, and increased activity levels of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX). Taken together, GB and BABA have great potential to enhance the thermotolerance of Chinese cabbage through higher photosynthesis performance, osmoprotection, and antioxidant enzyme activity.

Mechanisms of the end-plate potential noise and its implication for the neuromuscular junction anatomy.

We construct a compact model to mimic the membrane voltage response to the concentration of acetylcholine ([ACh]) which is mediated by the stochastic gating of acetylcholine (ACh) receptors. The patterns of the voltage depolarization against [ACh] as well as the accompanying voltage noises are presented. The mechanism of the voltage fluctuation that caused by the stochastic gating of receptors is explained. We consider that our results explain the frequently observed "end-plate (potential) noise" in physiology and electromyographic literature. These results, together with the requirements of evolution pressure on the motor units, explain reasonably the anatomical structure of the neuromuscular junction.

Resveratrol Improves Intestinal Morphology and Anti-Oxidation Ability in Deoxynivalenol-Challenged Piglets.

This study aimed to investigate the potential effects of resveratrol (RES) on intestinal function and oxidative stress in deoxynivalenol (DON)-challenged piglets. Twenty-four healthy Duroc × Yorkshire × Landrace weaned piglets at the age of 28 ± 1 days were randomly divided into four groups with six repetitions per group. The four groups were as follows: the control group (CON), fed with a basic diet; the RES group, fed with a basal diet + 300 mg/kg RES; the DON group, fed with a basal diet containing 2.65 mg/kg DON; and the DON + RES group, fed with a basal diet containing 2.65 mg/kg DON + 300 mg/kg RES. The results showed that the growth performance and intestinal function of DON-challenged piglets were significantly decreased (p < 0.05). Compared with the DON group, the average daily feed intake of piglets in the DON + RES group was significantly increased (p < 0.05). Additionally, dietary RES ameliorated DON-induced intestinal morphology impairment, as indicated by the increased (p < 0.05) jejunal villi height and the ratio of the jejunal villi height/crypt depth. Furthermore, after the addition of RES, the activities of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) in the jejunum mucosa were significantly increased, and the content of malondialdehyde (MDA) was significantly declined (p < 0.05). In addition, the level of reactive oxygen species (ROS) in the mitochondria was significantly reduced by RES, while the mitochondrial membrane potential in jejunum was significantly increased by RES (p < 0.05). However, there was no obvious difference between DON + RES and DON groups on average daily gain and the ratio of feed togain, except for the significant inhibition of average daily feed intake (p < 0.05). In conclusion, RES could effectively alleviate the DON-induced oxidative stress on weaned piglets, and reduce the damage to mitochondria and intestinal morphology, so as to improve the growth performance of piglets.

Effects of dietary tributyrin on intestinal mucosa development, mitochondrial function and AMPK-mTOR pathway in weaned pigs.

BACKGROUND: The objective of this experiment was to investigate the influence of dietary tributyrin on intestinal mucosa development, oxidative stress, mitochondrial function and AMPK-mTOR signaling pathway. METHODS: Seventy-two pigs were divided into two treatments and received either a basal diet or the same diet supplemented with 750 mg/kg tributyrin. Each treatment has six replicates of six pigs. After 14 days, 6 pigs from each treatment were selected and the jejunal samples were collected. RESULTS: Results showed that supplemental tributyrin increased (P < 0.05) villus height and villus height: crypt depth of weaned pigs. Pigs fed tributyrin had greater (P < 0.05) RNA/DNA and protein/DNA ratios than pigs on the control group. The mRNA levels of sodium glucose transport protein-1 and glucose transporter-2 in the jejunum were upregulated (P < 0.05) in pigs fed the tributyrin diet. Dietary tributyrin supplementation lowered (P < 0.05) the malondialdehyde and hydrogen peroxide (H2O2) content in jejunum, enhanced (P < 0.05) the mitochondrial function, as demonstrated by decreased (P < 0.05) reactive oxygen species level and increased (P < 0.05) mitochondrial membrane potential. Furthermore, tributyrin increased (P < 0.05) mitochondrial DNA content and the mRNA abundance of genes related to mitochondrial functions, including peroxisomal proliferator-activated receptor-γ coactivator-1α, mitochondrial transcription factor A, nuclear respiratory factor-1 in the jejunum. Supplementation with tributyrin elevated (P < 0.05) the phosphorylation level of AMPK and inhibited (P < 0.05) the phosphorylation level of mTOR in jejunum compared with the control group. CONCLUSIONS: These findings suggest that dietary supplementation with tributyrin promotes intestinal mucosa growth, extenuates oxidative stress, improves mitochondrial function and modulates the AMPK-mTOR signal pathway of weaned pigs.

Dietary Tributyrin Attenuates Intestinal Inflammation, Enhances Mitochondrial Function, and Induces Mitophagy in Piglets Challenged with Diquat.

The study evaluated the effects of butyric acid, in the form of tributyrin on the oxidative stress, inflammation, and mitochondrial function in diquat-challenged pigs. Twenty-four weaned pigs were allocated to four treatments in a 2 × 2 factorial arrangement with the main effects of tributyrin supplementation and diquat challenge. The results showed that supplemental tributyrin increased ( P < 0.05) average daily gain and average daily feed intake of diquat-challenged pigs. Tributyrin elevated ( P < 0.05) the activities of total antioxidant capacity and superoxide dismutase, reduced ( P < 0.05) malondialdehyde content, and increased ( P < 0.05) mRNA levels of copper and zinc superoxide dismutase and manganese-containing superoxide dismutase of diquat-challenged pigs. Tributyrin relieved ( P < 0.05) intestinal inflammation reflected by decreased mRNA abundances of tumor necrosis factor-α, interferon-γ, and interleukin-6 in the intestine. Tributyrin reduced ( P < 0.05) serum diamine oxidase activity and d-lactate content, increased ( P < 0.05) transepithelial electrical resistance, decreased paracellular flux of dextran (4 kDa), and prevented the diquat-induced decrease ( P < 0.05) in the expressions of claudin-1, occludin, and zonula occludens-1. Tributyrin alleviated ( P < 0.05) diquat-induced mitochondrial dysfunction shown by lowered reactive oxygen species, increased mitochondrial membrane potential, and increased adenosine triphosphate content. Furthermore, tributyrin increased ( P < 0.05) expressions of mitophagy proteins (PTEN-induced putative kinase 1 and Parkin), and ratio of light chain 3-II to light chain 3-I in intestine. Collectively, tributyrin attenuated oxidative stress and intestinal inflammation, improved mitochondrial function, and induced mitophagy in diquat-challenged pigs.

Resveratrol improves intestinal barrier function, alleviates mitochondrial dysfunction and induces mitophagy in diquat challenged piglets1.

This study evaluated whether resveratrol can alleviate intestinal injury and enhance the mitochondrial function and the mitophagy level in diquat induced oxidative stress of piglets. Twenty-four 35 day old piglets were randomly allocated to four groups: (1) nonchallenged control; (2) control + 100 mg kg-1 resveratrol diet; (3) diquat-treated control and (4) diquat + 100 mg kg-1 resveratrol diet. At the beginning of the experiment, the piglets were injected with diquat or saline (10 mg per kg bodyweight). On day 14, the piglets were killed to obtain the jejuna segments. The results showed that resveratrol increased (P < 0.05) the total antioxidant capacity (T-AOC) and decreased (P < 0.05) the hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in the jejunal mucosa, in comparison with the diquat group. Resveratrol improved (P < 0.05) the intestinal barrier function, as indicated by the increased transepithelial electrical resistance and the decreased paracellular permeability of fluorescein isothiocyanate dextran 4 kDa in the jejunum. Moreover, resveratrol prevented (P < 0.05) the diquat induced decline of occludin, claudin-1 and ZO-1 levels in the jejunal mucosa. Resveratrol ameliorated mitochondria swelling, vacuolation and cracked cristae induced by diquat. Resveratrol decreased (P < 0.05) the ROS generation and increased (P < 0.05) the membrane potential of intestinal mitochondria, the content of mitochondrial DNA and the activity of mitochondrial complexes I-IV in the jejunum. Finally, resveratrol enhanced (P < 0.05) the level of PTEN induced putative kinase 1 (PINK1) and Parkin in intestinal mitochondria; meanwhile it increased (P < 0.05) the LC3-II/LC3-I ratio in the jejunum. These data indicate that resveratrol is effective in protecting the intestinal barrier, improving the redox status, alleviating mitochondrial damage and inducing mitophagy in piglets challenged with diquat.