Understanding the dynamic evolution of hemicellulose during Pinus taeda L. growth.

Pinus taeda L. is a fast-growing softwood with significant commercial value. Understanding structural changes in hemicellulose during growth is essential to understanding the biosynthesis processes occurring in the cell walls of this tree. In this study, alkaline extraction is applied to isolate hemicellulose from Pinus taeda L. stem segments of different ages (1, 2, 3, and 4 years old). The results show that the extracted hemicellulose is mainly comprised of O-acetylgalactoglucomannan (GGM) and 4-O-methylglucuronoarabinoxylan (GAX), with the molecular weights and ratios (i.e., GGM:GAX) of GGM and GAX increasing alongside Pinus taeda L. age. Mature Pinus taeda L. hemicellulose is mainly composed of GGM, and the ratio of (mannose:glucose) in the GGM main chain gradually increases from 2.45 to 3.60 with growth, while the galactose substitution of GGM decreases gradually from 21.36% to 14.65%. The acetylation of GGM gradually increases from 0.33 to 0.45 with the acetyl groups mainly substituting into the O-3 position in the mannan. Furthermore, the contents of arabinose and glucuronic acid in GAX gradually decrease with growth. This study can provide useful information to the research in genetic breeding and high-value utilization of Pinus taeda L.

Attenuation of Perfluorooctane Sulfonate-Induced Steatohepatitis by Grape Seed Proanthocyanidin Extract in Mice.

Perfluorooctane sulfonate (PFOS), an environmentally persistent pollutant, has been revealed to elicit hepatic toxicity. In the current study, we investigated the protective role of grape seed proanthocyanidin extract (GSPE) against PFOS-caused steatohepatitis in mice. Animals were exposed intragastrically to PFOS (10 mg/kg/day), GSPE (150 mg/kg/day), or their combination. After 21 days of treatment, mice exposed to PFOS exhibited steatosis, oxidative stress, and inflammation in the liver. Nevertheless, simultaneous administration of GSPE resumed the declined serum hepatic enzyme activities and histological abnormalities in PFOS-exposed mice. Furthermore, GSPE supplementation reduced the contents of triglyceride (TG) and total cholesterol (TC) and expression of lipid metabolism-associated genes CD36 and fatty acid-binding protein 4 (FABP4) in the liver of mice treated with PFOS. Moreover, GSPE suppressed the generation of lipid peroxidative product malondialdehyde and restored the activity of superoxide dismutase in the liver of PFOS-exposed mice. In addition, GSPE repressed the PFOS-induced hepatic overproduction of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Our results demonstrate that GSPE attenuates PFOS-caused steatohepatitis in mice by regulating lipid metabolism, oxidative stress, and inflammatory response.