The effects of paeoniflorin on LPS-induced liver inflammatory reactions

Abstract

Paeoniflorin (PF), a monoterpene glucoside, is a primary bioactive component of paeony, the root extract of Paeonia lactiflora. We tested the antioxidant effects of PF and its ability to prevent lipopolysaccharide (LPS)-induced oxidative stress. We intraperitoneally administered PF (2.5, 5, or 10 mg/kg) to rats for 20 days. On day 21, we injected the rats with LPS 4 h before sacrifice and measured serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase as well as the levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase in liver whole-cell homogenates and mitochondrial fractions. LPS treatment increased levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, and malondialdehyde, but PF treatment blocked these increases. LPS treatment also decreased antioxidant levels of superoxide dismutase, catalase, and glutathione peroxidase, but PF blocked these decreases. PF also protected liver tissue, as shown by histopathology. These results suggest that PF can protect against LPS-induced liver inflammation.

Paeoniflorin inhibits function of synoviocytes pretreated by rIL-1α and regulates EP4 receptor expression

“…Paeoniflorin (Pae), a monoterpene glucoside, is one of the principal bioactive components of total glucosides of paeony (TGP) extracted from the root of Paeonia lactiflora. Pae has been verified to have anti-inflammatory (Fu et al, 2009;Jiang et al, 2009a,b;Huang et al, 2010;Kim and Ha, 2010;Tang et al, 2010;Cao et al, 2011), anti-allergic (Lee et al, 2008), analgesic , immunoregulatory (Hsu et al, 1997;Jiang et al, 2009a,b), neuroprotective (Cao et al, 2010;Mao et al, 2011) and antitumor effects . In addition, Pae was reported to induce the immune tolerance of mesenteric lymph node lymphocytes, apoptosis of T cells (Tsuboi et al, 2004), neuroprotection in cerebral ischemia (Liu et al, 2005a,b), and enhancement of cognition (Liu et al, 2006).…”

Mechanisms involved in the therapeutic effects of Paeonia lactiflora Pallas in rheumatoid arthritis

“…In vitro studies also demonstrated the protective effects of paeoniflorin against hydrogen peroxide (H 2 O 2 )-induced oxidative damage in human umbilical vein endothelial cells (HUVECs) by decreasing the production of intracellular reactive oxygen species and increasing the production of endogenous antioxidants [33]. The antioxidative effect of paeoniflorin on the LPS-induced liver inflammatory reactions was confirmed by in vivo studies [34]. The LPS-induced decreases in antioxidant levels of superoxide dismutase, catalase, and glutathione peroxidase could be reversed by paeoniflorin [34].…”

“…The antioxidative effect of paeoniflorin on the LPS-induced liver inflammatory reactions was confirmed by in vivo studies [34]. The LPS-induced decreases in antioxidant levels of superoxide dismutase, catalase, and glutathione peroxidase could be reversed by paeoniflorin [34]. Inflammation induces oxidative stress by producing oxidants like reactive oxygen species and nitric oxide.…”

Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

“…There is accumulating evidence that the administration of paeoniflorin (PF) can provide anti-inflammatory effects in a variety of animal models [8,12]. In the present study, we explored the protective effect of PF on ALI induced by intratracheal instillation of LPS in mice.…”

“…Paeoniflorin (PF), the major active constituent of TGP, has been reported to have many pharmacological effects, such as antiallergic [7], antiarthritic [8], hepatoprotective [9], and analgesic [10]. Recently, it was documented to be able to inhibit the properties systemic inflammatory responses in cecal ligation and puncture-induced sepsis [11], a main reason for ALI, protect against lipopolysaccharide (LPS)-induced liver inflammation, and prevent the adhesion between LPS-induced inflammatory endothelial cells and leukocytes [12,13]. Furthermore, it was proven to exhibit inhibitory effects on neuroinflammation, and analgesic effects through activating adenosine A1 receptor [14,15], which is beneficial for reducing PMN cell trafficking and microvascular permeability in LPS-induced lung injury [3].…”