Objective To observe the expression level of inhibitor of differentiation 2 (Id‐2) and matrix metalloproteinases‐9 (MMP‐9) in rectal cancer ,analysis the correlation of the expression level of them ,to study the relationship between the expression level of them and the clinical pathology indicators of rectal cancer .Methods Rectal cancer tissues and normal tissue adjacent to rec‐tal cancer were obtained from the rectal cancer resection of 56 patients with rectal cancer ,using immunohistochemical method to ob‐serve the expression level of Id‐2 and MMP‐9 in normal tissue adjacent to rectal cancer and rectal cancer and Spearman correlation test to detect the correlation between the expression level of Id‐2 and MMP‐9 ;then we analyzed the relationships between the ex‐pression level of Id‐2 and MMP‐9 and the index of rectal cancer clinical pathology .Results The positive expression rate of Id‐2 in the in rectal cancer tissues is more higher than that of normal tissue of adjacent to rectal cancer (73 .21% vs .48 .21% ,P<0 .05) . The positive expression rate of MMP‐9 in the in rectal cancer tissues is higher than that of normal tissue of adjacent to rectal cancer (71 .43% vs .44 .64% ,P<0 .05) .Spearman correlation test showed that there is the positive correlation between the expression level of Id‐2 and MMP‐9 (r=0 .393 ,P=0 .003) .The expression levels of Id‐2 and MMP‐9 in rectal cancer were correlated with the degree of tumor differentiation ,TNM stage and lymph node metastasis (P<0 .05) ,but had no differences between the elements of age and sex (P>0 .05) .Conclusion There is a close relationship between the expression levels of Id‐2 and MMP‐9 in rectal cancer and the occurrence and development of rectal cancer .Rectal cancer with the higher Id‐2 expression level may be the ways to achieve tumor invasion and metastasis through MMP‐9 as a facilitator .

Objective To investigate the effects of atorvastatin calcium on thyroid function,im-mune response and C-Jun N-terminal kinase/p38 mitogen-activated protein kinase(JNK/p38 MAPK)signaling pathway in rats with hypothyroidism.Methods A total of 30 healthy adult male SD rats were randomly divided into control group,hypothyroid group(PTU group)and atorvastatin calcium treatment group(ACT group),with 10 rats in each group.Rats in the PTU group and the ACT group were injected with PTU subcutaneously at the dorsum of the neck every day for 28 consecutive days;instead of PTU,rats in the control group were injected subcutaneously with 0.3 mL of saline.After 2 weeks of PTU treatment,rats in the ACT group were gavaged with 3 mL of atorvastatin calcium sa-line solution(containing 5 mg/kg of atorvastatin calcium),which was administered once daily;the control group was gavaged with an equal amount of saline in the same way.The body weight,food intake and water intake of rats were measured weekly.The histopathological changes of the thyroid gland were observed in histopathological sections of rats in each group.Enzyme-linked immunosor-bent assay(ELISA)was performed to determine the levels of triiodothyronine(T3),thyroxine(T4),thyroid stimulating hormone(TSH),interferon γ(IFN-γ)and interleukin-4(TL-4)in ser-um;quantitative reverse transcriptase polymerase chain reaction(qRT-PCR)was performed to de-tect the mRNA expression levels of IFN-γ,IL-10,Foxp3 and IL-4;western blot was performed to determine the levels of p-JNK/JNK and p-p38/p38 MAPK.Results Compared with control group,PTU-induced hypothyroidism rats showed a significant decrease in body mass and food and water consumption(P＜0.05).After 2 weeks of treatment with atorvastatin calcium,the body mass loss of PTU rats was inhibited,food and water consumption was improved,and the differences were sta-tistically significant(P＜0.05).Atorvastatin calcium was able to significantly increase the serum T3 and T4 levels and decrease the serum TSH level in hypothyroid rats(P＜0.05).Atorvastatin calcium treatment was able to significantly alleviate histopathological changes such as follicular cell proliferation and related hypertrophy induced by PTU,and increase follicular size(P＜0.05).Af-ter treatment with atorvastatin calcium,the spleen mass of PTU rats increased significantly,and the expression of IFN-γ mRNA in hypothyroid rats decreased significantly,but the expression levels of IL-10 mRNA,Foxp3 mRNA and IL-4 mRNA increased significantly(P＜0.05).After treatment with atorvastatin calcium,the levels of p-JNK/JNK and p-p38/p38 MAPK in thyroid tissue of hypo-thyroid rats decreased significantly(P＜0.05).Conclusion Atorvastatin calcium treatment for hy-pothyroidism has the function of promoting the normalization of thyroid hormone imbalance,balan-cing Th1/Th2 cytokines,and inhibiting the activation of JNK/p38 MAPK signaling pathway.

Objective To investigate the effects of atorvastatin calcium on thyroid function,im-mune response and C-Jun N-terminal kinase/p38 mitogen-activated protein kinase(JNK/p38 MAPK)signaling pathway in rats with hypothyroidism.Methods A total of 30 healthy adult male SD rats were randomly divided into control group,hypothyroid group(PTU group)and atorvastatin calcium treatment group(ACT group),with 10 rats in each group.Rats in the PTU group and the ACT group were injected with PTU subcutaneously at the dorsum of the neck every day for 28 consecutive days;instead of PTU,rats in the control group were injected subcutaneously with 0.3 mL of saline.After 2 weeks of PTU treatment,rats in the ACT group were gavaged with 3 mL of atorvastatin calcium sa-line solution(containing 5 mg/kg of atorvastatin calcium),which was administered once daily;the control group was gavaged with an equal amount of saline in the same way.The body weight,food intake and water intake of rats were measured weekly.The histopathological changes of the thyroid gland were observed in histopathological sections of rats in each group.Enzyme-linked immunosor-bent assay(ELISA)was performed to determine the levels of triiodothyronine(T3),thyroxine(T4),thyroid stimulating hormone(TSH),interferon γ(IFN-γ)and interleukin-4(TL-4)in ser-um;quantitative reverse transcriptase polymerase chain reaction(qRT-PCR)was performed to de-tect the mRNA expression levels of IFN-γ,IL-10,Foxp3 and IL-4;western blot was performed to determine the levels of p-JNK/JNK and p-p38/p38 MAPK.Results Compared with control group,PTU-induced hypothyroidism rats showed a significant decrease in body mass and food and water consumption(P＜0.05).After 2 weeks of treatment with atorvastatin calcium,the body mass loss of PTU rats was inhibited,food and water consumption was improved,and the differences were sta-tistically significant(P＜0.05).Atorvastatin calcium was able to significantly increase the serum T3 and T4 levels and decrease the serum TSH level in hypothyroid rats(P＜0.05).Atorvastatin calcium treatment was able to significantly alleviate histopathological changes such as follicular cell proliferation and related hypertrophy induced by PTU,and increase follicular size(P＜0.05).Af-ter treatment with atorvastatin calcium,the spleen mass of PTU rats increased significantly,and the expression of IFN-γ mRNA in hypothyroid rats decreased significantly,but the expression levels of IL-10 mRNA,Foxp3 mRNA and IL-4 mRNA increased significantly(P＜0.05).After treatment with atorvastatin calcium,the levels of p-JNK/JNK and p-p38/p38 MAPK in thyroid tissue of hypo-thyroid rats decreased significantly(P＜0.05).Conclusion Atorvastatin calcium treatment for hy-pothyroidism has the function of promoting the normalization of thyroid hormone imbalance,balan-cing Th1/Th2 cytokines,and inhibiting the activation of JNK/p38 MAPK signaling pathway.