Morroniside（25406-64-8）

Pharmacological effect 1. Effect on SH-SY5Y nerve cells Inflammation, apoptosis, oxidative stress injury, Ca2+overload, mitochondrial dysfunction and amino acid toxicity are the main causes of cerebral ischemia-reperfusion injury. Therefore, it can prevent and treat cerebral ischemia reperfusion injury by inhibiting cell apoptosis, blocking glutamate receptor, clearing free radicals, promoting the growth and repair of brain tissue, blocking Ca2+influx, reducing inflammatory reaction, etc. (1) Promoting the growth of SH-SY5Y nerve cells The size of the cell body area, the length of the axon, and the number of cells are important indicators to measure the cell growth. Monoside can increase the MTT metabolic rate of nerve cells, the length of cell axons, cell body area and cell count. It can be inferred that mononoside can increase the survival rate of SH-SY5Y cells, increase the number of cell growth, and promote the growth of SH-SY5Y nerve cells. (2) Inhibition of oxidative damage of SH-SY5Y nerve cells induced by H2O2 can inhibit the production of intracellular reactive oxygen species and NO induced by H2O2, increase the content of intracellular glutathione (GSH), and play the role of small molecular antioxidant. Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) belong to the same family of nerve factor growth. NGF can nourish neurons and regulate their growth, development, differentiation and expression. BDNF is a protein synthesized in the brain. It plays an important role in the survival, differentiation, growth, development, anti-injury and repair of neurons. Monoside can enhance the function of NGF and the expression of BNDF. It indicates that mononoside can resist the injury of SH-SY5Y nerve cells induced by H2O2, and the mechanism of action may be to promote the differentiation and regeneration of cells, improve the pathological state of nerve cells, repair damaged neurons and other ways to make some cells survive after stress injury. (3) Effect of mononoside on SH-SY5Y nerve cell apoptosis can prevent the decrease of mitochondrial membrane potential of SH-SY5Y cells induced by H2O2 injury, reduce the release of cytochrome C (Cyt-c), and reduce the activity of caspase-3. (4) Cell calcium overload, cytotoxicity and IL-1 in cerebral cortex β During cerebral ischemia and reperfusion, mononoside can inhibit the increase of intracellular free Ca2+, the influx of Ca2+caused by H2O2, the release of LDH and the IL-1 in brain tissue β To reduce brain tissue damage. Thus, when cerebral ischemia-reperfusion injury occurs, mononoside reduces and antagonizes the injury induced by ischemia by inhibiting the three mechanisms of calcium overload, inflammatory reaction and anti-cytotoxicity Chemicalbook. 2. Influence on blood viscosity, coagulation function and platelet aggregation. Blood viscosity, that is, blood viscosity, is often used as an index to prevent thrombosis such as cerebral stroke. Blood viscosity is directly proportional to blood flow resistance. The higher the viscosity, the greater the resistance, and the greater the influence on microcirculation perfusion. The experiment found that mononoside can effectively reduce the increase of blood viscosity caused by focal cerebral ischemia model. Monoside can resist the coagulation function of rats with focal cerebral ischemia and reperfusion, effectively improve blood viscosity and inhibit platelet aggregation. 3. Effect on myocardial cells Hyperglycemia can easily lead to myocardial cell damage, increase the level of oxidative stress, make the two cardiac enzymes of lactate dehydrogenase isoenzyme (LDH) and serum glutathione aminotransferase (GOT) flow out of the broken cell membrane into the blood, reduce the antioxidant function of SOD, induce free radical metabolism disorder, increase the content of MDA (malondialdehyde), and aggravate the damage of cell membrane. Monoside can resist the changes of cell morphology caused by high glucose, improve the survival rate of myocardial cells, reduce the content of LDH, GOT and MDA, and improve the activity of SOD. It can be speculated that mononoside can resist the injury caused by hyperglycemia by improving the antioxidant capacity of myocardial cells. 4. Melasma is a pigmented disease that inhibits the synthesis of melanin. Its formation is mainly related to the excessive synthesis of melanin. The oxidation reaction of tyrosine is the source of melanin formation. Tyrosinase is the main rate-limiting enzyme in the melanin biosynthesis pathway, and its activity determines the rate of melanin synthesis. Monoside can inhibit tyrosinase activity and presumably inhibit melanin synthesis by inhibiting tyrosinase activity. 5. Monoside can promote the release of intracellular calcium and the proliferation, differentiation and mineralization of osteoblasts. It can be concluded that mononoside can promote fracture healing. 6. Impact on diabetes nephropathy diabetes nephropathy is a serious complication of diabetes. Advanced glycation end products (AGEs) reduce and age the function of proteins, and damage to glomerular endothelial cells easily leads to prolonged insulin action, glomerulosclerosis, tubulointerstitial fibrosis, and destruction of glomerular filtration barrier. Therefore, AGEs and glomerular endothelial cell injury play a crucial role in the pathogenesis of diabetes nephropathy. Monoside can reduce the generation of AGEs, protect human umbilical vein endothelial cells (HUVEC) from high glucose induced injury, and reduce the levels of blood sugar, urine protein, serum albumin and total protein in diabetes rats. 7. Other pharmacological activities of mononoside improve the abnormal differentiation of adipocytes; Significantly promote the proliferation of lymphocytes; Suppress PTP-1B; It is also one of the effective material bases of Liuwei Dihuang Pill for tonifying the kidney.

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