最新刊期
期 3 ， 2022
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- 摘要：ObjectiveTo investigate the hypoglycemic effect of Tangfukang Formula on KK-Ay mice and its complex biological network relationship with intestinal flora.MethodsTwenty-four 8-week-old SPF KK-Ay spontaneous diabetes model mice were randomly divided into 4 groups，namely model group，Tangfukang high-dose group，equivalent dose group and metformin group，with 6 mice in each group. Six C57BL/6J mice were used as normal control group. Normal control group and model group were given normal saline with intragastric administration，Tangfukang high-dose group，equivalent dose group and metformin group were given Tangfukang of 6.4 and 3.2 g/kg·d and metformin of 250 mg/kg·d with intragastric administration respectively. After 1 month of intervention，the sample was got and the blood glucose was detected，the pathological degree of skeletal muscle cells was observed under light microscope，and the structure of intestinal microflora of mice was analyzed by 16S rDNA sequencing.ResultsTangfukang Formula could effectively reduce blood glucose，alleviate inflammatory infiltration and atrophy and necrosis of skeletal muscle，and significantly increase the diversity of intestinal flora，increase the relative abundance of bacteroidetes and decrease the relative abundance of firmicutes in mice.ConclusionTangfukang Formula has a good hypoglycemic effect on KK-Ay mice，and its antidiabetic effect may be related to the regulation of intestinal microflora structure.关键词：Tangfukang Formula;diabetic KK-Ay mice;intestinal microflora
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发布时间：2023-02-15 - 摘要：ObjectiveTo observe effects of Tangluoning on inflammatory reaction of Schwann cells induced by high glucose in vitro with lncRNA MALAT1 as the starting point and explore the possible mechanism of protecting Schwann cells.MethodsWith Schwann cells of rats as objective，cell injury model was established by high glucose stimulation. They were randomly divided into 4 group：normal group（blank serum culture），high glucose group （blank serum culture + 150 mmol/L glucose），Tangluoning group （medicine serum culture + 150 mmol/L glucose）and lncRNA MALAT1 knockout group（150 mmol/L glucose + MALAT1 inhibitor）. The cells of each group were collected and detected after 48 hours. Cells viability was determined by CCK-8 assay. Expression of lncRNA MALAT1 and inflammatory factors （IL-6，MCP-1 and TNF-α）were assessed by real-time PCR or enzyme linked immunosorbent assay.ResultsCompared with the normal group，the cell viability of high glucose group was reduced （P<0.05），the gene and protein expression of inflammatory factors （IL-6，MCP-1 and TNF-α） were increased （P<0.05），the expression of MALAT1 was increased（P<0.05）；compared with high glucose group，the cell viability of both Tangluoning group and MALAT1 knockout group was increased（P<0.05），the gene and protein expression of inflammatory factors were decreased （P<0.05），the expression of MALAT1 of Tangluoning group was more decreased than that of the high glucose group （P<0.05）.ConclusionTangluoning could alleviate inflammatory reaction of Schwann cell induced by high glucose through inhibiting the expression of lncRNA MALAT1．关键词：Tangluoning;Schwann cell;lncRNA MALAT1;inflammatory reaction;rat
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发布时间：2023-02-15 -
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- 摘要：ObjectiveTo study the protective effect of Jiedu Liangxue Formula on D-galactose （D-GalN） combined with lipopolysaccharide （LPS） induced acute liver failure in mice and its mechanism.Methods30 mice were randomly divided into normal group，model group and Jiedu Liangxue Formula group with 10 mice in each group. Except for normal group，acute liver failure model was induced by intraperitoneal injection of D-GalN（400 mg/kg） and LPS（0. 25 mg/kg） in the other two groups. The Jiedu Liangxue Formula group was gavaged 500 μL Jiedu Liangxue Formula immediately after the injection of the model agent，and the model group and the normal group were gavaged with the same volume of double steamed water. After 5 hours of modeling，the heart blood was collected and liver tissue samples were kept. Liver function （including serum alanine aminotransferase（ALT），aspartate aminotransferase （AST），total bilirubin （TBIL），direct bilirubin （DBIL），albumin （propagated），cholinesterase （CHE）were tested by automatic biochemical analyzer，the liver tissue pathology change was observed by wood grain - eosin（HE） staining，liver cell apoptosis rate was detected by TUNEL，the protein expressions of caspase-9，caspase-3，glycoprotein 2（SGP-2），Bcl-2 and Bax in mitochondrial apoptosis pathway of liver cells were detected by Western blot，and mRNA expressions of SGP-2，Bcl-2 and Bax were detected by reverse transcriptase polymerase chain reaction（PCR）.ResultsCompared with normal group，serum levels of ALT，AST，TBIL and DBIL in model group were significantly increased，CHE was significantly decreased（P< 0.05），the liver pathological damage was obvious，apoptosis cells were significantly increased（P<0.05），the expression of SGP-2，Bax and cleaved caspase-9 and caspase-3 were high，and the expression of Bcl-2 was low （P<0.05）；compared with model group，the levels of ALT，AST，TBIL and DBIL in serum of Jiedu Liangxue Formula group were significantly decreased（P<0.05），the pathological damage of liver tissue was mild，and the apoptosis rate of liver cells was low（P<0.05），SGP-2，Bax and cleaved caspase-9 and cleaved caspase-3 were expressed at low level，and Bcl-2 expression was at high level（P<0.05）.ConclusionJiedu Liangxue Formula has treatment effect on D-GalN/ LPS-induced acute liver failure in mice，and its mechanism may be related to the inhibition of hepatocyte apoptosis mediated by mitochondrial apoptosis signaling pathway.关键词：Acute liver failure;mitochondrial apoptosis signaling pathway;Jiedu Liangxue Formula;mouse
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发布时间：2023-02-15 - 摘要：ObjectiveTo investigate the mechanism of Shumai Capsule in inhibiting intimal hyperplasia after iliac artery intervention in rats.Methods28 rats were randomly divided into sham operation group，model group，Shumai Capsule group and FABP4 inhibitor group，with 7 rats in each group. In the sham-operated group，only skin and muscularis incision was performed，but balloon traction was not performed. The model group，Shumai Capsule group and FABP4 inhibitor group were treated with percutaneous transluminal coronary angioplasty（PTCA）catheter，and the left iliac artery was injured through the left femoral artery to establish the lower extremity artery restenosis model. On the second day after operation，Shumai Capsule group was given 0.068 g/mL Shumai Capsule suspension by gavage，and the FABP4 inhibitor（BMS309403）group was given intraperitoneal injection of 1.6 mg/kg，the sham operation group and model group were given normal saline by gavage. After 6 weeks，the intimal thickness and lumen diameter of left iliac artery were detected by small animal Doppler ultrasound，and the levels of NO and FABP4 in serum were detected by ELISA. The expression of FABP4 protein in left iliac artery was detected by Western blotting.ResultsThe intima of model group，Shumai Capsule group and FABP4 inhibitor group was thickened and the thickness and lumen diameter of them were significantly larger than that of sham group（P<0.05），the thickness of Shumai Capsule group was less than that of model group（P<0.05）. The content of NO in model group，Shumai capsule group and FABP4 inhibitor group was lower than that in sham group（P<0.05）；the content of NO in Shumai capsule group and FABP4 inhibitor group was higher than that in model group （P<0.05）；the content of FABP4 in Shumai Capsule group and FABP4 inhibitor group was lower than that in model group（P<0.05）. The FABP4 protein in left iliac artery in Shumai capsule group and FABP4 inhibitor group was lower than that in model group （P<0.05）.ConclusionShumai Capsule can improve vascular endothelial function by down regulating of FABP4，increase the production of NO，and inhibit intimal hyperplasia.关键词：Peripheral artery disease;postoperative restenosis;intimal hyperplasia;Shumai Capsule;rat
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发布时间：2023-02-15 -
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- 摘要：ObjectiveTo study the protective effect of Shenfu Injection（SFI） on cardiotoxicity caused by adriamycin chemotherapy.MethodsThe cardiomyocytes H9c2 cells of rat were cultured in vitro and treated with different drugs. They were divided into several treatment groups： doxorubicin groupu，SFI grouup，SFI and doxorubicin combination group，and physiological saline control group. Cell apoptosis，mitochondrial oxidative damage，ROS level and activation of apoptosis caspase-3 were evaluated to study the molecular mechanism of Shenfu injection on cardiomyocyte protection.ResultsSFI can significantly inhibit the cardiomyocyte apoptosis caused by doxorubicin，reduce the production of ROS，and mitigate mitochondrial oxidative injury so as to play a protective role.ConclusionSFI certainly has a certain protective effect on heart injury caused by doxorubicin.关键词：Shenfu injection;Doxorubicin;cardiotoxicity;oxidative stress
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发布时间：2023-02-15 -
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