Objective To Observe the influence of Zaoshi Jiedu Zhupi Sanjing (ZPSJ) Recipe on insulin sensitivity, serum resistin and inflammatory factors related to the effects of Chinese herbal compound in type 2 diabetic patients with insulin resistance. Methods A single-blind randomized controlled clinical trial was conducted. 80 patients with 2 type diabetic patients with insulin resistance were recruited into a control group and a treatment group. The treatment group was treated with ZPSJ Recipe, and the control group was treated with metformin. Results In each group before and after treatment: blood glucose, serum insulin levels, HOMA-IR were significantly decreased (t=7.14, P<0.01 ) ; between the two groups, FPG, FINS showed no significant difference, while TG TCH, HOMA-LR showed significantly differences (t=2.62, P <0.05 ). Within the two groups before and after the treatment: serum IL-6, TNF-a, hs-CRP were decreased in treatment group, (t= 1.85, P<0.05 ) , while TNF-a, hs-CRP were decreased in the control group (t=2.56, P<0.05 ) , while IL-6 did not change significantly. The serum resistin levels were not statistically changed in both groups before and after treatment. Conclusion ZPSJ Recipe can regulate blood sugar, blood fat and improve insulin sensitivity in type 2 diabetic patients with insulin resistance.

Objective: To establish sporadic Alzheimer's disease (SAD) rat model, to investigate the effects of Xixin Decoction Granule (XDG) on the phosphorylation of Thr231 and Ser422 sites as the important promoters of Tau protein toxicity in the brain of SAD rat, and to explore the possible mechanism of XDG on the prevention and treatment of SAD. Methods: The SPF male SD rats were randomly divided into Sham (S), model (M), donepezil (D, positive control), low-, mid-, and high-dose XDG (LX, MX, and HX, 7.61, 15.21, and 30.42 g/kg) groups, with ig administration once daily for two months. The immunohistochemistry and Western blotting were used to detect the phosphorylation levels of Thr231 and Ser422 sites in Tau protein in brain of rats with SAD. Results: Compared with M group, XDG could significantly decrease the expression of Thr231 and Ser422 sites in the hippocampus of SAD rats (P < 0.05, 0.01). There were no obvious differences between D and M groups (P > 0.05). Conclusion: The results suggest that XDG could inhibit the hyperphosphorylation of key sites in site protein and Tau toxicity, so as to prevent SAD pathological progress.

This study aimed to explore the possible effect of Xixin Decoction(XXD) on the learning and memory ability of Alzheimer's disease(AD) model senescence-accelerated mouse-prone 8(SAMP8) and the related mechanism in enhancing neuroprotective effect and reducing neuroinflammation. Forty SAMP8 were randomly divided into a model group(10 mL·kg~(-1)·d~(-1)), a probiotics group(0.39 g·kg~(-1)·d~(-1)), a high-dose group of XXD granules(H-XXD, 5.07 g·kg~(-1)·d~(-1)), a medium-dose group of XXD granules(M-XXD, 2.535 g·kg~(-1)·d~(-1)), and a low-dose group of XXD granules(L-XXD, 1.267 5 g·kg~(-1)·d~(-1)). Eight senescence-accelerated mouse-resistant 1(SAMR1) of the same age and strain were assigned to the control group(10 mL·kg~(-1)·d~(-1)). After ten weeks of intragastric administration, the Morris water maze was used to test the changes in spatial learning and memory ability of mice after treatment. Meanwhile, immunofluorescence staining was used to detect the positive expression of receptor for advanced glycation end products(AGER), Toll-like receptor 1(TLR1), and Toll-like receptor 2(TLR2) in the hippocampal CA1 region of mice. Western blot was employed to test the protein expression levels of silencing information regulator 2 related enzyme 1(SIRT1), AGER, TLR1, and TLR2 in the hippocampus of mice. Enzyme linked immunosorbent assay(ELISA) was applied to assess the levels of Aβ_(1-42) in the hippocampus of mice and the levels of nuclear factor κB p65(NF-κB p65), NOD-like receptor protein 3(NLRP3), tumor necrosis factor-α(TNF-α), and interleukin-1β(IL-1β) in the serum and hippocampus of mice. Compared with the model group, XXD significantly improved the spatial learning and memory ability of SAMP8, increased the expression of neuroprotective factors in the hippocampus, decreased the levels of neuroinflammatory factors, and inhibited the expression of Aβ_(1-42). In particular, H-XXD significantly increased the expression of SIRT1 in the hippocampus of mice, reduced the expression levels of NF-κB p65, NLRP3, TNF-α, and IL-1β in the serum and hippocampus of mice, and decreased the expression of AGER, TLR1, and TLR2 in the hippocampus of mice(P<0.05 or P<0.01). XXD may improve the spatial learning and memory ability of AD model SAMP8 by enhancing the neuroprotective effect and inhibiting neuroinflammation.
Humans ; Neuroprotective Agents/therapeutic use* ; Sirtuin 1/metabolism* ; Toll-Like Receptor 2/metabolism* ; NF-kappa B/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Neuroinflammatory Diseases ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Toll-Like Receptor 1/metabolism* ; Alzheimer Disease/genetics* ; Hippocampus