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Functional dyspepsia (FD) is a common disease in clinics. It is necessary to establish suitable animal models for clarifying the pathogenesis of FD. FD belongs to "Piman" (abdominal disten- sion) , "Weiwantong" (epigastric pain) , "Caoza" (epigastric upset) in Chinese medicine (CM). It is inor- ganic disease but functional disease. There is no unified standard for FD animal models. Pi deficiency syndrome model is often used as FD animal model now, but they are not completely the same thing. Au- thors summarized and analyzed common methods for FD modeling.

Aim: To investigate the effect and the possible mechanism of ginsenoside Rb1 on small intestinal smooth muscle motility in mice., Methods: Intestinal smooth muscle strips were isolated from male ICR mice (5 wk old), and the effect of ginsenoside Rb1 on spontaneous contraction was recorded with an electrophysiolograph. The effect of ginsenoside Rb1 on ion channel currents, including the voltage-gated K⁺ channel current (IK(V)), calcium-activated potassium channel currents (IK(Ca)), spontaneous transient outward currents and ATP-sensitive potassium channel current (IK(ATP)), was recorded on freshly isolated single cells using the whole-cell patch clamp technique., Results: Ginsenoside Rb1 dose-dependently inhibited the spontaneous contraction of intestinal smooth muscle by 21.15% ± 3.31%, 42.03% ± 8.23% and 67.23% ± 5.63% at concentrations of 25 μmol/L, 50 μmol/L and 100 μmol/L, respectively (n = 5, P < 0.05). The inhibitory effect of ginsenoside Rb1 on spontaneous contraction was significantly but incompletely blocked by 10 mmol/L tetraethylammonium or 0.5 mmol/L 4-aminopyridine, respectively (n = 5, P < 0.05). However, the inhibitory effect of ginsenoside Rb1 on spontaneous contraction was not affected by 10 μmol/L glibenclamide or 0.4 μmol/L tetrodotoxin. At the cell level, ginsenoside Rb1 increased outward potassium currents, and IK(V) was enhanced from 1137.71 ± 171.62 pA to 1449.73 ± 162.39 pA by 50 μmol/L Rb1 at +60 mV (n = 6, P < 0.05). Ginsenoside Rb1 increased IK(Ca) and enhanced the amplitudes of spontaneous transient outward currents from 582.77 ± 179.09 mV to 788.12 ± 278.34 mV (n = 5, P < 0.05). However, ginsenoside Rb1 (50 μmol/L) had no significant effect on IK(ATP) (n = 3, P < 0.05)., Conclusion: These results suggest that ginsenoside Rb1 has an inhibitory effect on the spontaneous contraction of mouse intestinal smooth muscle mediated by the activation of IK(V) and IK(Ca), but the K(ATP) channel was not involved in this effect.

Objective: To investigate the abnormal change of immune function in patients with Pi-Qi deficiency Syndrome, and to explore the genomic mechanism of its genesis by cDNA chip techniques., Methods: The cross probe was made by extracting and microamplifying the total RNA and mRNA of peripheral white blood cells (WBC) in healthy subjects and patients with chronic gastritis and ulcerative colitis, which were labeled by Cy3 and Cy5 respectively. Then equal quantity of the two labeled probes were mixed and hybridized with cDNA chip, fluorescent signal of the chips were scanned with scanner. Data obtained were analyzed for comparing the difference of the expressive levels of immune associated genome in peripheral WBC in healthy subjects with those in patients., Results: Expressions of CD9, CD164, PF4 and RARB gene in WBC of patients, both gastritis and colitis, were down-regulated while those of IGKC, DEFA1 and GNLY were up-regulated., Conclusion: The genesis of Pi-Qi deficiency syndrome has its immune associated genomic basis, and the immune functions are disordered in patients with that syndrome.