<p>Biogenic selenium nanoparticles synthesized by <em>Lactobacillus casei</em> ATCC 393 alleviate intestinal epithelial barrier dysfunction caused by oxidative stress via Nrf2 signaling-mediated mitochondrial pathway</p>

Abstract

Background: Selenium (Se) can exert antioxidative activity and prevent the body from experiencing oxidative injury. Biogenic Se nanoparticles (SeNPs) synthesized by probiotics possess relatively strong chemical stability, high bioavailability, and low toxicity, this makes them potential Se supplements. Previously, we demonstrated that SeNPs synthesized by Lactobacillus casei ATCC 393 can alleviate hydrogen peroxide (H 2 O 2 )-induced human and porcine intestinal epithelial cells' oxidative damage. However, the antioxidant mechanism remains unclear. Methods: The possible antioxidant mechanism and protective effect of SeNPs on intestinal epithelial permeability and mitochondrial function were evaluated by establishing an H 2 O 2 -induced oxidative damage model of human colon mucosal epithelial cells (NCM460) and conducting Nrf2 inhibitor interference experiments. Mitochondrial membrane potential (MMP), mitochondrial DNA content, adenosine triphosphate (ATP), ROS, and protein expression levels of Nrf2-related genes were determined. Mitochondrial ultrastructure was visualized by transmission electron microscopy. Results: An amount of 4 μg Se/mL of SeNPs synthesized by L. casei ATCC 393 alleviated increase of ROS, reduced ATP and MMP, and maintained intestinal epithelial permeability in NCM460 cells challenged by H 2 O 2 . In addition, SeNPs improved the protein levels of Nrf2, HO-1, and NQO-1. Moreover, SeNPs attenuated the damage of mitochondrial ultrastructure caused by oxidative stress. Nrf2 inhibitor (ML385) abolished the regulatory effect of SeNPs on intracellular ROS production. Conclusion: Data suggest that biogenic SeNPs synthesized by L. casei ATCC 393 can protect the intestinal epithelial barrier function against oxidative damage by alleviating ROS-mediated mitochondrial dysfunction via Nrf2 signaling pathway. Biogenic SeNPs are an attractive candidate for potential Se supplement agent in preventing oxidative stress-related intestinal disease by targeting mitochondria.

Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species

“…The NRF2/HO-1 signaling pathway serves a vital role in oxidative stress. Under homeostatic conditions, NRF2 is not functionally activated and exists in the cytoplasm; however, once cells are subjected to oxidative stress, NRF2 is translocated into the nucleus and combines with the antioxidant response element to trigger HO-1 expression, thereby regulating the expression of oxidant or antioxidant-related genes and enzymes, such as SOD and MDA, and finally exerting its antioxidant defense function (35). Therefore, strengthening the antioxidant process may be considered a potential strategy to reduce the level of cellular necroptosis, in order to reduce the extent of tissue damage.…”

Oxidative stress tolerance and antioxidant capacity of lactic acid bacteria as probiotic: a systematic review

“…LAB can alleviate oxidative stress-induced mitochondrial dysfunction via Nrf2 signaling, strengthening the epithelial barrier function. 99 enhancing the antioxidant defense response. 112 In another study in mammalian cells, it was discovered that LG2055 treatment activated JNK, and inhibition of JNK activation suppressed Nrf-2 ARE signaling activation and the protective effect of LG2055 against oxidative stress.…”

<p>Nitroxide-Modified Protein-Incorporated Nanoflowers with Dual Enzyme-Like Activities</p>

“…It can be further speculated that the hybrid nanoflowers could act as a prospectively useful tool for controlling oxidative stress, similar to the antioxidant properties of other nanomaterials, which have been already been investigated in existing studies. [32][33][34][35][36][37]…”