## 3 Pharmacological Properties of GP
### Hepatoprotective Effects
\begin{table}
\begin{tabular}{c c c c c} \hline \hline \multirow{2}{*}{**Models**} & \multicolumn{2}{c}{**Medicinal Composition**} & \multirow{2}{*}{**Dosage**} & \multirow{2}{*}{**Activity/Mechanism**} & \multirow{2}{*}{**Ref.**} \\ \hline CCl4-induced liver injury & & & & Decreased the level of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), down-regulated the \\ in rats & GPP & 30 days, i.g. & iiNOS mRNA expression in hepatic tissue, elevated the level of Bcl-2/Bax in hepatic \\  & & & tissue and alleviated liver injury. & \\ \hline CCl4-induced chronic & & & Reduced the activities of serum glutamic \\ liver injury in rats & & & transaminase and serum glutamic pyruvate \\  & & & transaminase, elevated albumin/globulin \\  & & 8 weeks, 4 times per & ratio, prevented CCl4-induced liver damage, \\  & & week, p.o. & reduced the collagen content, suppressed the \\  & & & onset and enhanced the recovery of liver \\  & & & fibrosis induced by CCl4. & \\ CCl4-induced acute liver & & & Decreased the level of serum ALT, \\  & injury in rats & GPS & 100 mg/kg, i.v. & ameliorated liver injury. & \\ \hline CCl4-induced liver & & & Ameliorated CCl4-induced liver fibrosis via \\  & & & the inhibition of TGF-\(\beta\) signaling, \\  & fibrosis in rats & GPS & weeks, i.g. & consequently inhibited the differentiation of \\  & & & hepatic progenitor cells into myofibals. & \\ \hline Exhaustive & & & Increased the expression of Bcl-2 and \\  & & & decreased the expression of Bax, increased \\  & & & SOD, GSH-Px, and CAT activities and \\  & & & decreased MDA contents in liver, exerted \\  & & & protective effect on oxidative stress and \\  & & & apoptosis induced by exhaustive exercise. & \\ \hline Alcohol-induced liver & & & Decreased the level of MDA and increased \\  & injury in rats & GPS & 50, 100, and 200 mg/kg \\  & & & for 7 days, i.g. & improved the level of inflammatory \\  & & & system by activating the Nrf signaling \\  & & & pathway, reduced the level of inflammatory \\  & & & cytokines TNF-\(\alpha\) and IL-6 by inhibiting the \\  & & & nuclear transposition of NF-kB. & \\ \hline High choline-induced & & & Elevated T-SOD and GSH-Px activity, \\  & & & decreased the MDA concentration, alleviated \\  & & & 800 mg/kg for \\  & & & 8 weeks, i.g. & the high choline-induced oxidative stress \\  & & & injury, lowered the levels of AST and ALT. & \\ \hline  & & & Decreased the levels of serum TG, TC, LDL-C, \\  & & & free fatty acid, increased HDL-C level, \\  & & & increased SOD activity, reduced MDA level \\  & & & and ALT and AST activities, prevented liver \\  & & & fatty degeneration through up-regulation of \\  & & & PPAR-\(\alpha\) expression in the liver to inhibit lipid \\  & & & peroxidation and hepatocyte apoptosis, \\  & & & ameliorated hepatic steatosis and damage, \\  & & & and improved hepatic function. \\ \hline Methionine choline & & & Reduced hepatic fat accumulation, \\  & & & hepatocellular injury, inflammation, and \\  & & & fibrosis, increased the expression of SIRT6 \\  & & & and phase 2 anti-oxidant enzymes, and then \\  & & & attenuated oxidative stress in the liver. & \\ \hline \hline \end{tabular}
\end{table} 
Table 5: Hepatoprotective effects of GP.