Guanxinning tablets improve myocardial hypertrophy by inhibiting the activation of MEK-ERK1/2 signaling pathway.

Myocardial hypertrophy may lead to heart failure and sudden death. As traditional Chinese medicine, Guanxinning tablets (GXN) have significant pharmacological effects in the prevention and treatment of cardiovascular diseases. However, the anti-cardiac hypertrophy efficacy of GXN and its mechanism of action are still unclear. Therefore, we established a heart failure rat model and isolated primary cardiomyocytes of neonatal rat to observe the protective effect of GXN on heart failure rat model and the intervention effect on myocardial cell hypertrophy, and to explore the possible mechanism of GXN preventing and treating myocardial hypertrophy. The results of in vivo experiments showed that GXN could significantly reduce the degree of cardiac hypertrophy, reduce the size of cardiomyocytes, inhibit the degree of myocardial remodeling and fibrosis, and improve cardiac function in rats with early heart failure. The results of in vitro experiments showed that GXN was safe for primary cardiomyocytes and could improve cardiomyocyte hypertrophy and reduce the apoptosis of cardiomyocytes in pathological state, which may be related to the inhibition of the over-activation of MEK-ERK1/2 signaling pathway. In conclusion, GXN may inhibit cardiac hypertrophy and improve early heart failure by inhibiting the over-activation of MEK-ERK1/2 signaling pathway.

Guanxinning tablet inhibits the interaction between leukocyte integrin Mac-1 and platelet GPIbα for antithrombosis without increased bleeding risk.

Recent studies have showed that thrombosis is closely related to leucocytes involved in immunity. Interfering with the binding of leukocyte integrin Mac-1 and platelet GPIbα can inhibit thrombosis without affecting physiological coagulation. Mac-1-GPIbα is proposed as a potential safety target for antithrombotic agents. Guanxinning tablet (GXNT) is an oral Chinese patent medicine used for the treatment of angina pectoris, which contains phenolic acid active ingredients, such as salvianolic acids, ferulic acid, chlorogenic acid, caffeic acid, rosmarinic acid, tanshinol, and protocatechualdehyde. Our previous studies demonstrated that GXN exhibited significant antithrombotic effects, and clinical studies suggested that it did not increase bleeding risk. In addition, GXN exerted a significantly regulatory effect on immune inflammation. In the current study, we intended to evaluate the effects of GXN on bleeding events and explore the safety antithrombotic mechanism of GXN based on leukocyte-platelet interaction. First, we established a gastric ulcer model induced by acetic acid in rats and found that GXN not only did not increase the degree of gastrointestinal bleeding when gastric ulcer occurred, but also had a certain promoting effect on the healing of gastric ulcer. Second, in vitroexperiments showed that after pretreatment with GXN and activation by phorbol 12-myristate-13-acetate (PMA), the adhesion and aggregation of leukocytes with human platelets were reduced. It was also found that GXN reduced the expression and activation of Mac-1 in leucocytes, and inhibited platelet activation due to leukocyte engagement via Mac-1. Overall, the results suggest that GXN may be a safe antithrombotic agent, and its low bleeding risk mechanism is probably related to inhibited leukocyte-platelet aggregation and its interaction target Mac-1-GPIbα.

Semaphorin 7a participants in pterygium by regulating vascular endothelial growth factor.

AIM: To investigate the relationship between semaphorin 7a expression and cell proliferation and migration in pterygium fibroblasts. METHODS: Twenty-six patients with surgically diagnosed pterygium were enrolled, including 15 cases of primary pterygium and 11 cases of recurrent pterygium. In addition, 12 cases of normal conjunctival tissue were collected. The expression of semaphorin 7a in normal conjunctival tissue, primary pterygium and recurrent pterygium was detected by real-time polymerase chain reaction. Recurrent pterygium fibroblasts were isolated and cultured, and the expression of semaphorin 7a was silenced by small interfering RNA (siRNA) interference technique. Furthermore, the effects of si-semaphorin 7a interference on the mRNA and protein levels of ß1-integrin, vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptor (VEGFR), and on fibroblast proliferation were analyzed. Transwell assay was used to detect the effect of semaphorin 7a interference on fibroblast migration. RESULTS: Semaphorin 7a was highly expressed in the primary pterygium and recurrent pterygium samples than that of the normal conjunctival tissue. Compared with the primary pterygium, the expression of semaphoring 7a in the recurrent pterygium samples was significantly increased (P<0.05). The mRNA and protein expression levels of ß1-integrin, VEGFA and VEGFR were decreased after si-semaphorin 7a transfection, and as well as the cell proliferation and migration. CONCLUSION: Semaphorin 7a might play important roles in the pathogenesis of pterygium by affecting the expression of ß1-integrin, VEGFA and VEGFR.

Corrigendum to "A Review of Collagen Cross-Linking in Cornea and Sclera".

[This corrects the article DOI: 10.1155/2015/289467.].

A review of collagen cross-linking in cornea and sclera.

Riboflavin/UVA cross-linking is a technique introduced in the past decades for the treatment of keratoconus, keratectasia, and infectious keratitis. Its efficacy and safety have been investigated with clinical and laboratory studies since its first clinical application by Wollensak for the treatment of keratoconus. Although its complications are encountered during clinical practice, such as infection inducing risk, minimal invasion merits a further investigation on its future application in clinical practice. Recently, collagen cross-linking in sclera shows a promising prospect. In present study, we summarized the representative studies describing the clinical and laboratory application of collagen cross-linking published in past decades and provided our opinion on the positive and negative results of cross-linking in the treatment of ophthalmic disorders.

Clinical significance of vascular endothelial growth factor and connexin43 for predicting pancreatic cancer clinicopathologic parameters.

Vasiformation is essential for the growth and metastasis of tumor. Vascular endothelial growth factor (VEGF) and connexin43 (Cx43) are important regulatory factors of vasiformation. This study aimed to find out the expression features of VEGF and Cx43 and their significance in pancreatic cancer. The expression levels of VEGF and Cx43 protein in the samples, which came from 100 patients of human pancreatic cancer tissues and adjacent normal pancreatic tissues, were examined by using immunohistochemical streptavidin-peroxidase (S-P) method, Western-blotting, and RT-PCR analyses. Compared with adjacent normal pancreatic tissues, RT-PCR showed that the expression of VEGF mRNA was significantly higher in pancreatic cancer tissues (0.788±0.290, P<0.01) and Cx43 mRNA was significantly lower in pancreatic cancer tissues (0.403±0.204, P<0.01). The expression of VEGF protein was higher in pancreatic cancer tissue (0.745±0.254, P<0.01) by Western-blot, and Cx43 protein was obviously lower in pancreatic cancer tissues (0.373±0.164, P<0.01). The immunohistochemical S-P method showed as follows: the positive expression rate of VEGF and Cx43 protein was 77 and 48% in pancreatic cancer tissues and 15 and 100% in adjacent normal pancreatic tissues; expressions of VEGF were related to tumor size, TNM stage, and lymph node metastasis (P<0.05); there was a close relation between the expression of Cx43 and histological grades, TNM stage, and lymph node metastasis (P<0.05). This present study suggests that VEGF is overexpressed and the expression of Cx43 is lower in pancreatic cancer. The expression of VEGF and Cx43 is significantly correlated with TNM stage and lymph node metastasis. Furthermore, VEGF and Cx43 may play an important role in the occurrence, development, and metastasis of pancreatic cancer. To examine VEGF and Cx43 may be of value in judging the malignancy degree and the prognosis of pancreatic cancer.

[Expression of vascular endothelial growth factor and metastin in colorectal carcinoma].

OBJECTIVE: To study the expression of vascular endothelial growth factor (VEGF) and metastin in colorectal carcinoma and their association with the clinicopathological features of the malignancy. METHODS: VEGF and metastin expressions were examined immunohistochemically with SP method in 70 specimens of human colorectal carcinoma tissues and adjacent normal tissues. RESULTS: VEGF protein overexpression was detected in 48.6% (34/70)of the colorectal carcinoma tissues but in none of the adjacent normal tissues (P<0.01), and for metastin, the overexpression rate was 28.6% (20/70) in the colorectal carcinoma tissues and 70.0% (49/70) in the normal tissues (P<0.01). The expression of both VEGF and metastin was related to the histological grades, infiltration depth, TNM stage and lymph node metastasis of the tumor (P<0.01 and P<0.05, respectively). CONCLUSION: Immunohistochemical detection of VEGF and metastin can be of value in assessment of the malignancy and in prognostic evaluation of colorectal carcinoma.

[Significance of MOC-31 and CD56 detection in human lung carcinoma tissues].

BACKGROUND & OBJECTIVE: The majority of research found that the positive rate of MOC-31 is higher in lung carcinoma than that in pleural mesothelioma. So MOC-31 is regarded as an important factor in differentiating diagnosis of lung carcinoma from pleural mesothelioma. But there are also few contrary reports. CD56 (neural cell adhesion molecule) is a sensitive factor in diagnosis of small cell lung carcinoma (SCLC), but the reports about its diagnostic sensitivity in non-small cell lung carcinoma (NSCLC) are different. This study was conducted to investigate the significance of MOC-31 and CD56 in diagnosis of human lung carcinoma. METHOD: Immunohistochemical method (S-P) was used to detect MOC-31 and CD56 expression in 92 cases of lung carcinoma. RESULT: The positive rate of MOC-31 in lung carcinoma was 98.9% (91/92), among which, 98.6% (72/73) in NSCLC, 100% (19/19) in SCLC; the positive expression rate of CD56 in lung carcinoma was 30.4% (28/92), among which, 12.3% (9/73) in NSCLC, 100% (19/19) in SCLC. MOC-31 and CD56 expressions in adjacent lung tissue and normal lung tissue were negative. CONCLUSION: MOC-31 is an antibody which is highly sensitive and peculiar to lung carcinoma, whereas CD56 only showed sensitive to SCLC. Therefore, combined determination of MOC-31 and CD56 is more useful than that of single item in diagnosing SCLC.