Cinobufacini Inhibits the Development of Pancreatic Cancer Cells through the TGFß/Smads Pathway of Pancreatic Stellate Cells.

This study aimed to test cinobufacini therapeutic potential for pancreatic cancer, verify its potential molecular mechanism, and evaluate the cinobufacini impact on pancreatic cancer microenvironment. First, the effect of cinobufacini-treated pancreatic stellate cells (PSCs) supernatant on the value-added ability of pancreatic cancer (PCCs) was tested. The results show that cinobufacini can effectively reduce the ability of PSCs supernatant to promote the value-added PCCs. Further results show that cinobufacini can effectively reduce the concentration of TGFß in the supernatant of PSCs. Subsequently, the impact of cinobufacini on the transcription and translation levels of key genes in the TGFß/Smads pathway was examined. The results showed that the impact of cinobufacini on the transcription levels of Smad2, Smad3, and Smad7 was in a concentration-dependent manner, while the transcriptional activity of collagen I mRNA was decreased with the increase of cinobufacini concentration. The results of protein expression showed that cinobufacini could upregulate the expression of inhibitory protein Smad7, inhibit the phosphorylation level of p-Smad2/3, and then suppress the expression of type I collagen (collagen I). On the one hand, this study shows that cinobufacini can inhibit the promotion of PSCs on the proliferation of PCCs. On the other hand, cinobufacini can upregulate the expression of the inhibitory molecule, Smad7, through the TGFß/Smads pathway and reduce the phosphorylation level of p-Smad2/3, thereby inhibiting the expression of collagen I and pancreatic fibrosis. cinobufacin can inhibit the proliferation of SW1900 cells by blocking the TGFß/Smads pathway of pancreatic stellate cells. These results provide a clinical basis for the treatment of pancreatic cancer.

Regulating effect of activated NF-κB on edema induced by traumatic brain injury of rats

OBJECTIVE@#To observe the effect of nuclear transcription factor-κB (NF-κB) on cerebral edema in rats with traumatic brain injury (TBI).@*METHODS@#Male SD rats with fluid percussion injury (FPI) were selected. After separation and culture, rats' astrocytes all suffered FPI. The expression of NF-κB and the water content were detected at the animal and cellular levels, while the activity of NOX was evaluated at the cellular level.@*RESULTS@#According to the results, the positive expression of NF-κB and expression of mRNA were significantly increased and the water content was increased for rats after TBI, while NF-κB inhibitor BAY11-7082 could significantly reduce the effect of TBI. 1 and 3 h after FPI of astrocytes, the activation of NF-κB was increased and BAY 11-7082 could significantly improve the injury-induced swelling of astrocytes. After the injury of astrocytes, the activity of NOX was also increased, while BAY 11-7082 could reduce the activity of NOX.@*CONCLUSIONS@#The results show that the activation of NF-κB in astrocytes is a key factor in the process of cerebral edema after TBI of rats.

Regulating effect of activated NF-κB on edema induced by traumatic brain injury of rats

Objective: To observe the effect of nuclear transcription factor-κB (NF-κB) on cerebral edema in rats with traumatic brain injury (TBI). Methods: Male SD rats with fluid percussion injury (FPI) were selected. After separation and culture, rats' astrocytes all suffered FPI. The expression of NF-κB and the water content were detected at the animal and cellular levels, while the activity of NOX was evaluated at the cellular level. Results: According to the results, the positive expression of NF-κB and expression of mRNA were significantly increased and the water content was increased for rats after TBI, while NF-κB inhibitor BAY11-7082 could significantly reduce the effect of TBI. 1 and 3 h after FPI of astrocytes, the activation of NF-κB was increased and BAY 11-7082 could significantly improve the injury-induced swelling of astrocytes. After the injury of astrocytes, the activity of NOX was also increased, while BAY 11-7082 could reduce the activity of NOX. Conclusions: The results show that the activation of NF-κB in astrocytes is a key factor in the process of cerebral edema after TBI of rats.

Two new compounds from the flowers of Rhododendron molle / 中国天然药物

AIM@#To study the chemical constituents of the flowers of Rhododendron molle.@*METHODS@#Compounds were isolated by repeated chromatography over silica gel and Sephadex LH-20. Structures were elucidated based on spectral techniques, mainly 1D- and 2D-NMR and mass spectrometric analyses.@*RESULTS@#Two compounds (1 and 2) were isolated.@*CONCLUSIONS@#Compounds 1 and 2 were identified as two new compounds: 2α, 10α-epoxy-3β, 5β, 6β, 14β, 16α-hexahydroxy-grayanane and benzyl 2, 6-dihydroxybenzoate-6-O-α-L-rhamnopyranosyl-(1→3)-β-D-glucopyranoside, respectively.

Phenolic glucosides from the leaves of Pieris japonica / 药学学报

The aim of the study is to investigate chemical constituents of the leaves of Pieris japonica. The isolation and purification of the constituents were performed by various chromatography and spectral analysis. Three new phenolic glucosides, erythro-syringoylglycerol 4-O-beta-D-glucoside (1), 1-(2-beta-D-glucopyranoxyl-4-methoxyl-6-hydroxyphenyl)-3-hydroxyl-l-propanone (3), erythro-l-(4-hydroxyl-3-methoxyphenyl)-2-[4-(3-beta-D-glucopyranoxypropyl)-2 ,6-dimethoxyphenoxy]-1, 3-propanediol (4), along with five known phenolic glucosides, syringoylglycerol 8-O-beta-D-glucoside (2), magnolenin C (5), syringaresinol mono-beta-D-glucoside (6), 3-(4-hydroxyl-3-methyphenyl)-1 -propanol-l-O-beta-D-glucoside (7) and 3, 5-dimethoxyl-4-hydroxybenzyl alcohol 4-O-beta-D-glucoside (8) were isolated and identified from the plant leaves. Compounds 1 and 2 inhibited significantly (P <0.01) the proliferation of murine T and B cells at concentration of 1 x 10(-6) mol L(-1), in vitro.

Clinical observation on the combined treatment of 57 cases of non-small cell lung cancer using argon-helium cryosurgery and Chinese herbal medicine.

OBJECTIVE: To observe the clinical effect of the combined therapy using argon-helium cryosurgery (Ar-He knife) and Chinese herbal medicine in treating non-small cell lung cancer (NSCLC). METHODS: Fifty-seven patients of NSCLC were treated with the combined therapy and observed. RESULTS: The treatment was successfully completed in all patients with mild adverse reactions. The effective rate was 83.8% 3 months after the operation, 79.6% 6 months after the operation, and 77.3% 12 months after the operation, with median survival of 9 months. The survival rate after 12 months was 46.67% (21/45), 34.62% (9/26) after 18 months, and 36.36% (4/11) after 24 months. CONCLUSION: Argon-helium cryosurgery therapy is superior in its assured orientation, quick tumor load deprivation and less postoperational reaction. Combined with Chinese herbal medication, Argon-helium cryosurgery therapy can prolong survival time, relieve clinical symptoms, and elevate the quality of life in NSCLC patients, and is thus worthy of promotion.

Detecting microdeletions of the Y chromosome in patients with high follicle-stimulating hormone azoospermia / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To explore the relationship between the patients' high follicle-stimulating hormone (FSH) azoospermia and microdeletions in Y chromosome.</p><p><b>METHODS</b>Eleven sequence tagged sites (STSs) in Yq were detected by PCR in 16 male patients' high FSH azoospermia.</p><p><b>RESULTS</b>Microdeletions were observed in 6 of 16 male patients and the deletion rate was 37.5%(6/16). Five types of microdeletions were detected: AZFc(SY152), AZFc (SY152+SY254)+AZFd (SY153), AZFc (SY152+SY254+SY255)+AZFd (SY153), AZFc (SY152+SY158+SY255)+AZFd (SY153),and AZFb (SY130)+AZFc (SY158+SY254+SY255)+AZFd (SY153) respectively.</p><p><b>CONCLUSION</b>Microdeletion of Y chromosome was one of the important reasons of the patients' high FSH azoospermia. Before the application of assisted-reproductive technology (ART) to the patients, it is necessary to detect the microdeletions, especially AZFc and AZFd.</p>