Objective To observe the effects of Qishu granule on PI3K/Akt signaling transduction pathways in the process of hepatic fibrosis, and further explain the anti-hepatic fibrosis mechanism of Qishu granule.Methods Wistar rats were randomly divided into normal group, model group, experimental control group and Qishu granule group. Liver fibrosis was duplicated in rats by intraperitoneal injection of CCl4, and the rats were given appropriate treatment at the same day. Rats in Qishu granule group were given a gavage 2 g/(kg?d), 1.0 mL/100 g, while rats in experimental control group and normal group were given the same amount of aquae sterilisata. Rats in each group were taken liver tissue samples in the 1st, 2nd and 4th week, and were checked for the protein expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 by Western blot.Results Compared with the model group, expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 in model and Qishu granule groups increased in every time points (P<0.05). Compared with the model group, expression level of p-Akt (Ser473) in Qishu granule group decreased significantly in the 1st, 2nd, and 4th weeks, expression level of Caspase9 dropped in the 1st and the 4th weeks, with statistical significance (P<0.05,P<0.01);expressions of p-Akt (Thr308) and Bad (Ser136) were lower than those in model group, without statistical significance (P>0.05).Conclusion Qishu granule could regulate PI3K/Akt signaling transduction pathways, and inhibit the occurrence and development of liver fibrosis.

OBJECTIVE: To establish a rat model of cervical syndrome (CS) with kidney deficiency. METHODS: A group of 30 three-month-old female Sprague-Dawley rats were randomly divided into normal control group, CS group and CS with kidney deficiency group (combined group), with 10 rats in each group. Rats in the normal control group received no treatment, rats in the CS group underwent only resection of cervical muscles and ligaments as unbalanced dynamic and static animal model, and rats in combined group underwent resection of both cervical muscles and ovaries as kidney deficiency model. Serum and cervical intervertebral discs were collected. Kidney deficiency was determined by observing the morphologic changes of uterus and appendages, detecting the weight of uterus and appendages and the content of serum estradiol (E(2)). The degeneration of intervertebral discs was determined by detecting the histopathology, the expressions of type II collagen and type X collagen proteins, and the expressions of aggrecan-1 (Agc1), type II procollagen gene (Col2a1), matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNAs. RESULTS: Compared with those in the normal control group and CS group, the rats in the combined group were noted with the uterus atrophied, the caliber of oviduct thinned, the weight of uterus and appendages diminished obviously, the content of serum E(2) decreased, cervical intervertebral disc degenerated more seriously, type II collagen protein expression decreased, type X collagen protein expression increased, Agc1 and Col2a1 mRNA expressions in intervertebral disc decreased, and the MMP-13 mRNA expression increased. CONCLUSION: The rat model of CS with kidney deficiency is established. Kidney deficiency can aggravate cervical intervertebral disc degeneration.

To establish a rat model of cervical syndrome with qi deficiency, blood stasis and kidney deficiency.