A review of edible plant-derived natural compounds for the therapy of liver fibrosis.

Liver fibrosis has a high incidence worldwide and is the common pathological basis of many chronic liver diseases. Liver fibrosis is caused by the excessive deposition of extracellular matrix and concomitant collagen accumulation in livers and can lead to the development of liver cirrhosis and even liver cancer. A large number of studies have provided evidence that liver fibrosis can be blocked or even reversed by appropriate medical interventions. However, the antifibrosis drugs with ideal clinical efficacy are still insufficient. The edible plant-derived natural compounds have been reported to exert effective antifibrotic effects with few side-effects, representing a kind of promising source for the treatment of liver fibrosis. In this article, we reviewed the current progress of the natural compounds derived from dietary plants in the treatment of liver fibrosis, including phenolic compounds (capsaicin, chlorogenic acid, curcumin, ellagic acid, epigallocatechin-3-gallate, resveratrol, sinapic acid, syringic acid, vanillic acid and vitamin E), flavonoid compounds (genistein, hesperidin, hesperetin, naringenin, naringin and quercetin), sulfur-containing compounds (S-allylcysteine, ergothioneine, lipoic acid and sulforaphane) and other compounds (betaine, caffeine, cucurbitacin B, lycopene, α-mangostin, γ-mangostin, ursolic acid, vitamin C and yangonin). The pharmacological effects and related mechanisms of these compounds in in-vivo and in-vitro models of liver fibrosis are focused.

Evaluation of a modified rat model for functional dyspepsia.

Background/Aim: The purpose of this study was to establish a modified rat model with functional dyspepsia (FD) and analyze the changes in gastrointestinal motility and brain-gut peptide levels in serum and brain-gut axis. Materials and Methods: Male Wistar rats were divided into control group (Con) and FD model group. FD model was established by stimulating semi-starvation rats via tail damping, provocation, and forced exercise fatigue until gastrointestinal motility disorder appeared, and then levels of motilin, leptin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) were detected in serum by enzyme linked immunosorbent assay and in duodenum, antrum, and hypothalamus by immunohistochemistry, reverse transcriptase-polymerase chain reaction, and Western blot. Results: The results showed rates of intestinal propulsion and gastric emptying slowed down markedly compared to Con (P < 0.05), the gastrointestinal electric activity attenuated, and migrating motor complex (MMC) interrupted in the model group. The levels of leptin and VIP markedly increased, but motilin decreased as compared to the Con (P < 0.05) in serum and in the above tissues. It is interesting that the level of CCK decreased in the antrum and duodenum but increased in the hypothalamus as compared to Con (P < 0.05). Conclusions: The modified rat model meets the diagnostic criteria of FD and can be used as a method for studying FD in animals.

Pingwei capsules improve gastrointestinal motility in rats with functional dyspepsia.

OBJECTIVE: To investigate the mechanism of Pingwei capsules (PWC) in improving gastrointestinal motility in rats with functional dyspepsia (FD). METHODS: We established an FD model by stimulating semi-starvation rats via tail damping, provocation, and forced exercise fatigue. The FD model group was further divided into five groups according to the treatment received: normal saline, domperidone, low-dose PWC, mid-dose PWC, or high- dose PWC. The effect of PWC on FD rat was evaluated by measuring gastrointestinal motility. Changes of leptin and cholecystokinin (CCK) were detected through enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and immunohistochemistry. RESULTS: PWC significantly increased gastrointestinal motility in FD rats. Furthermore, PWC significantly increased CCK mRNA and protein concentrations in the duodenum and antrum, decreased leptin protein concentrations in the duodenum, antrum, and hypothalamus, and decreased CCK protein concentration in the hypothalamus. CONCLUSION: PWC improve gastrointestinal motor function in FD rats by decreasing the leptin concentration in serum and the brain-gut axis, and by increasing the CCK concentration in gastrointestinal tissue. Our findings help to elucidate the mechanism of FD and provide further insight into the pharmacokinetics of PWC.