On a single hand, it influences lipoprotein-mediated cholesterol transport in the bloodstream, and alternatively it gains NF-κB1/p50 Gene ID serum-dependent efflux of cellular cholesterol. The potential of PACs and (+)-catechin from red wine to primarily bind to Apo A-I in humans and transferrin in rats additional corroborates an involvement of PACs in reverting cholesterol transport [347]. Going deeper into the molecular particulars of PACs action it has been observed that they affect ROS, glutathione (GSH), and MDA intracellular levels [208,314]. Oligomers decrease the generation of ROS and lipid peroxidation and improve the decreased glutathione/oxidized glutathione ratio [208]. In addition, PACs can modulate the activity of many crucial antioxidant enzymes which includes glutathione peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD) [314,348]. In this context, EGCG therapy promotes Nfr2 nuclear accumulation and transcriptional activity [349]. This action comes from theAntioxidants 2021, 10,37 ofactivation on the Akt and ERK1/2 signaling pathways and results in the modulation in the antioxidant response element (ARE)-mediated expression of lots of antioxidants as well as detoxifying enzymes. These activities, collectively using the restoration of lipid regulatory enzyme-like 5′ adenosine monophosphate-activated protein kinase (AMPK) and ACC phosphorylation [278], lead to an improvement in lipid peroxidation damage ultimately resulting in serum LDL/HDL ratio lowering. 7.3. Intestinal Inflammation Intestinal inflammatory illnesses are contemporary circumstances of industrialized societies. Their enhanced incidence has been associated using the westernization of diet plan and atmosphere, with strong alterations in intestinal microbiota, and with continuous intestinal epithelial cell exposure to pesticides, food additives, drugs, along with other food chemicals [35052]. To date, sufficient tactics for the RSK2 Source prevention or therapy of inflammatory gut diseases are still lacking. Several studies have evaluated the influence of dietary components inside the prevention and treatment of intestinal inflammation and protective effects of a number of polyphenols had been reported [165]. In particular, rising data from in vitro and in vivo studies showed protective effects of proanthocyanidins on intestinal epithelium supporting positive effects of PACs and PAC rich-foods for the physiology of the gastrointestinal tract. The primary manuscripts describing the anti-inflammatory potential derived in the intake of PACs are reported in Tables four and 5. Several in vivo studies (Table 5), using murine models of experimental colitis, showed that PACs have anti-inflammatory effects in intestinal bowel diseases (IBD). Oral administration of PAC-rich extracts results in significant protection against epithelial barrier dysfunctions [35355], mainly exerted by way of the inhibition of TNF-, INF-, and IL-1 release, lowered myeloperoxidase activity [310,35557], inhibition of NF-B signaling pathway [35860], and elevated antioxidant enzymes (GPx and SOD) activity [361]. Regardless of these research revealing a possible valuable function of PACs in intestinal inflammation, the mechanisms involved within this protective effect have not yet been fully clarified. One of the mechanisms involved undoubtedly concerns the antioxidant properties of PACs: Wu et al. showed that incubation of intestinal epithelium with proanthocyanidin dimers prevented LPS-mediated oxidative tension rising SOD, HO-1, CAT, and GSH-Px mR.