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Objective To observe effects of different dosages of moxibustion with ginger-separated moxibustion on expressions of mitogen extracellular kinase (MEK) 1/2 and extracellular regulated protein kinase (ERK) 1/2 of gastric tissue in rats with spleen deficiency; To explore the possible mechanism and the dose-effect relationship. Methods Seventy-five SD rats were randomly divided into blank control group, model group, ginger-separated moxibustion for three zhuang group, six zhuang group and nine zhuang group according to random digits table method, with fifteen rats in each group. The rat model of spleen deficiency was established by intragastric administration with 200% Rhei Radix et Rhizoma infusion at 4 ℃. Ginger-separated moxibustion groups were treated with different dosage of moxibustion at "Zusanli", "Zhongwan" for eight days after the modeling. Pathological changes of gastric tissue by HE staining were observed under light microscope, and immunohistochemistry was used to detect the expressions of MEK1/2 and ERK1/2 protein in gastric tissue of rats. Results Compared with the blank control group rats, the gastric mucosa injury in the model group was obvious, which showed that the damage and abscission was more serious; compared with the model group, the gastric mucosa of rats was partly exfoliated and the damage was improved in three zhuang group, and the surface of gastric mucosa of rats was more complete and damage was improved obviously in six zhuang group and nine zhuang group; compared with the blank control group, the expressions of MEK1/2 and ERK1/2 protein in gastric tissue increased obviously in other groups (P<0.01);compared with three zhuang group, the expressions of MEK1/2 and ERK1/2 protein in gastric tissue increased in six zhuang group and nine zhuang group (P<0.01), but the effects of the two group were similar, without statistical significance (P>0.05). Conclusion Ginger-separated moxibustion can repair gastric mucosa in rats with spleen deficiency, which may be closely associated with its effect in increasing the expressions of MEK1/2 and ERK1/2 protein in gastric tissue and activating the MEK/ERK signal transduction pathway.
RESUMEN
<p><b>OBJECTIVE</b>To observe the improvement of thyroid function and changes of Akt, p-Akt, mammalian target of rapamycin (mTOR), and para-mTOR (p-mTOR) expression in Graves' disease (GD) mice after intervened by Jiakangning Capsule (JC), and to explore possible mechanism for JC in treating GD.</p><p><b>METHODS</b>GD model was established by immunizing female BALB/c mice with thyroid stimulating hormone receptor A subunit (Ad-TSHRα-289). Totally 70 successfully modeled mice were divided into the model group (n =20), the JC intervened group (n =25), the Methimazole Tablet intervened group (n =25) according to random digit table. A normal control group (n =15) and a vehicle control group (n =20, injected with Ad-null) were also set up. Mice in the JC intervened group were administered with JC suspension at the daily dose of 1. 5 g/kg by gastrogavag. Mice in the Methimazole intervened group were administered with Methimazole suspension at the daily dose of 2. 5 g/kg by gastrogavage. Equal volume of normal saline was administered to mice in the rest 3 groups by gastrogavage. All intervention lasted for 5 weeks. Six mice were selected from each group to observe pathological changes of thyroid tissues. Serum levels of thyroxine (T4), triiodothyronine (T3), thyroid stimulating hormone (TSH), and thyrotropin receptor antibody (TRAb) were analyzed by radioimmunoassay. Expression levels of Akt, p-Akt, mTOR, and p-mTOR in thyroid tissues were etermined by Western blot.</p><p><b>RESULTS</b>(1) The thyroid gland in the GD model group showed proliferative changes, with enlarged follicles of various sizes. Interstitial stroma was filled with blood vessels. Structures of thyroid tissues in the JC intervened group and the Methimazole intervened group were significantly restored, and follicular hyperplasia was relieved. (2) Compared with the normal control group and the vehicle control group, levels of TRAb, T4, and T3 increased; ratios of P-Akt/β-actin, p-Akt/Akt, p-mTOR/β-actin, and p-mTOR/mTOR also increased in the model group (all P <0. 01). Compared with the model group, levels of TRAb, T4, and T3 decreased in the JC intervened group and the Methimazole intervened group (P <0. 01); ratios of p-mTOR/β-actin and pmTOR/mTOR decreased in the JC intervened group (P <0.01); ratios of P-Akt/β-actin, p-Akt/Akt, p-mTOR/β-actin, and p-mTOR/mTOR decreased in the Methimazole intervened group (P <0. 05, P <0. 01). Conclusion JC could reduce thyroid hormonc levels of GD mice and lower expression levels of mTOR, and its mechanism for improving thyroid function of GD mice might be associated with this influence.</p>