Effects of polysaccharide from Physalis alkekengi var. francheti on liver injury and intestinal microflora in type-2 diabetic mice

Abstract

Context: Diabetic liver injury is a serious diabetic complication. The alterations of intestinal microbiota play an important role in induction and promotion of liver injury progression. Physalis alkekengi L. var. francheti (Mast.) Makino (Solanaceae) has been used as a water decoction for treating diabetes.

Objective: To study the effects of a polysaccharide (PPSB) from Physalis alkekengi var. francheti on liver injury and intestinal microflora in type-2 diabetic mice.

Materials and methods: Streptozotocin (160 mg/kg) was injected i.p. for 3 days to build model. The diabetic mice were randomly divided into four groups together with control group (10 mice in each group). The doses of PPSB were 50 and 100 mg/kg, respectively. After 5 weeks administration, level of blood glucose, ALT and AST were measured. Alterations of intestinal microflora, and protein expression of TGF-β1, TNF-α and DCN were detected.

Results: Level of blood glucose decreased from (25.38 ± 2.21) mmol/L to (18.01 ± 2.53) mmol/L, ALT and AST decreased to (24.67 ± 4.86) U/L and (30.84 ± 7.50) U/L in PPSB-H group. Lactobacillus, Clostridium butyricum, and Bacteroides increased remarkably with increasing concentration of PPSB, but Enterobacter was inhibited. The relative expression of TGF-β1 and TNF-α decreased to (0.70 ± 0.17) and (0.39 ± 0.06), and the expression of DCN increased to (0.65 ± 0.13).

Discussion and conclusions: Probiotics have been promoted by PPSB, and protein expressions have been modulated in the progression of liver injury. PPSB could be used as a natural agent for treating diabetic liver injury and intestinal microflora imbalance.

Keywords: Antidiabetic effects; diabetic liver injury; dominant organisms; protein expression.

Figure 1.

Levels of blood glucose (A), ALT and AST (B) of normal and streptozotocin-induced diabetic mice (X¯ ± s, n = 10). ^ΔΔp < 0.01, ^Δp < 0.05 vs. the blank control group (N); **p < 0.01, *p < 0.05 vs. the diabetic model group (D). N: normal mice treated with water; L: diabetic mice with 50 mg/kg of PPSB; H: diabetic mice with 100 mg/kg of PPSB; D: diabetic mice with distilled water; E: diabetic mice with 600 mg/kg of dimethylbiguanide.

Figure 2.

Representative DGGE profiles (A) and UPGMA dendrograms (B) of blank control, diabetic mice, diabetic mice with 50 and 100 mg/kg of PPSB, and positive control groups. Group 1: Blank control group (N), normal mice treated with water. Group 2: Diabetic model group (D), diabetic mice with distilled water. Group 3: Diabetic mice with 600 mg/kg of dimethylbiguanide. Group 4: Diabetic mice with 50 mg/kg of PPSB (L). Group 5: Diabetic mice with 100 mg/kg of PPSB (H).

Figure 3.

Effects of PPSB on expression of TGF-β1, TNF-α, and DCN in livers. **p < 0.01, *p < 0.05 vs. the blank control group (N); ^ΔΔp < 0.01, ^Δp < 0.05 vs. the diabetic model group (D). N: normal mice treated with water; L: diabetic mice with 50 mg/kg of PPSB; H: diabetic mice with 100 mg/kg of PPSB; D: diabetic mice with distilled water; E: diabetic mice with 600 mg/kg of dimethylbiguanide.