Platycodin D isolated from the aerial parts of Platycodon grandiflorum protects alcohol-induced liver injury in mice

Abstract

Platycodin D (PD) is the main active saponin of Platycodon grandiflorum (PG) and is reported to exhibit multiple biological effects, including anti-tumor, anti-inflammation, and anti-obesity properties. Although recently there have been many research reports on the chemical constituents of the plant's roots, only few works have been reported on the aerial parts of PG. In the present study, we report the first isolation of PD from the aerial parts of PG and its protective effect against acute alcohol-induced liver oxidative injury and inflammatory response in mice. In brief, the protective effect was evaluated by tracking biochemical markers, enzymatic antioxidants and proinflammatory cytokines in serum and liver tissue. The results indicated that PD pretreatment significantly decreased the levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (L-DLC) in serum and malondialdehyde (MDA) in liver. PD was also found to increase the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in the liver (p < 0.05). In addition, PD markedly decreased the levels of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, which was caused by alcohol exposure (p < 0.05). In contrast, histopathological examinations revealed that PD pretreatment noticeably prevented alcohol-induced hepatocyte apoptosis and steatosis. Collectively, the present study clearly suggests that the protective effect exhibited by PD on alcohol-induced liver oxidative injury may occur via the alleviation of oxidative stress and inflammatory response.

Natural compounds in the chemoprevention of alcoholic liver disease

“…Platycodin D supplementation promoted activities of antioxidant enzymes, including CAT, SOD, and GSH‐Px (Liu et al, ). Another work also observed that platycodin D treatment reversed the elevated levels of ALT, AST, thereby corroborating results observed in the paper of Li et al (; Wu et al, ).…”

“…The work by Wu et al () uncovered the anti‐inflammatory activity of platycodin D on alcohol‐induced fatty livers. They also found that platycodin D treatment reversed the elevated levels of inflammatory cytokines, including TNF‐α and IL‐6 induced by alcohol (Li et al, , Wu et al, ). In addition, they observed that platycodin D apparently inhibited ethanol‐induced elevation of plasma endotoxin, hinting at its potential protective role against endotoxemia induced by ethanol.…”

“…Platycodin D supplementation decreased the levels of pro‐inflammatory factors such as TNF‐α, IL‐1β, and IL‐6 (Li et al, ). The work by Wu et al () uncovered the anti‐inflammatory activity of platycodin D on alcohol‐induced fatty livers.…”

Curcumin‐galactomannosides mitigate alcohol‐induced liver damage by inhibiting oxidative stress, hepatic inflammation, and enhance bioavailability on TLR4/MMP events compared to curcumin

“…The inflammatory cascade and oxidative stress play major roles in alcohol‐induced hepatotoxicity . The antioxidant defense systems essentially include SOD, CAT, and GSH‐related enzymes, which were reported to decrease on ethanol administration . Accordingly, a significant decrease in the levels of SOD, CAT, GSH, and GPx activities was observed in the liver of the ethanol‐administered group of animals.…”

Platycodin D exerts anti-tumor efficacy in H22 tumor-bearing mice via improving immune function and inducing apoptosis

“…Platycodin D (PD, Fig. 1), the major active constituent of P. grandiflorum, has received more and more attention due to its pharmaceutical effects, including anti-inflammation (Chung et al, 2008;Zhang et al, 2015), anti-obesity (Zhao et al, 2006), anti-atherosclerosis (Wu et al, 2012), hepatoprotective Li et al, 2015a), and anti-tumor (Luan et al, 2014;Zhao et al, 2015) effects. It is worth mentioning that PD exerts remarkable anti-cancer effects on different kinds of cancer cell lines, including HepG2, MDA-MB-231, U937, K562, PC3, and MCF-7, with main molecular mechanisms such as promoting apoptosis and inhibiting migration and invasion (Tang et al, 2014;Li et al, 2014;Yu and Kim, 2010;Shin et al, 2009;Kim et al, 2008).…”