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Research of anti-inflammatory and neuroprotective effects of ginsenoside CK

Miao Jianchun

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Abstract

Objective To observe the anti-inflammatory and neuroprotective effects of ginsenoside CK and to investi gate the mechanism of action.Methods ①Lipopolysaccharide(LPS) induced murine sepsis model was copied,the ef fects of ginsenoside CK on brain microglia changes,tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were observed.②Rat models of cerebral ischemia reperfusion injury was duplicated,the effects of ginsenoside CK on the infarct volume percentage and microglial cell change were observed.③ Microglial cells were primary cultured to observe the effects of ginsenoside CK on LPS induced cell activation and culture medium of nitric oxide(NO) content and intracellular reactive oxygen species(ROS) content changes.Results ①TNF-α and IL-1β in model control group [(198.38±12.84) mg/L,(845.15±41.97) ng/L] were higher than those in normal control group [(106.71 ±11.21) mg/L,(477.46±49.76) ng/L],positive control group [(141.46±11.91) mg/L,(690.94±54.71) ng/L] and ginsenoside CK low level group [(157.23 ±12.25) mg/L,(726.04 ±64.29) ng/L],middle level group [(136.58 ±13.17) mg/L,(651.88 ±55.65) ng/L],high level group [(121.33±12.09) mg/L(577.36±51.86) ng/L],the differences were statistically significant(P 0.05 or P 0.01).②Lectin positive cell numbers of focal cerebral ischemia-reperfusion injury in rats in ginsenoside CK low level group [(30±7) numbers/500 μm2],middle level group [(20±5) numbers/500 μm2] and high level group [(13±4) numbers/500 μm2] were all lower than those in model group [(46±11) numbers/500 μm2],the differences were statistically significant(P 0.05 or P 0.01).Compared with model group,the infarct volume percentages in the ginsenoside CK low level group,middle level group,high level group significantly reduced(P 0.05 or P 0.01).③NO concentration of cell cultures in ginsenoside CK low level group [(18.16 ±0.59) mol/L],middle level group [(12.43 ±0.52) mol/ L] and high level group [(6.17±0.34) mol/L] were all lower than those in LPS group [(23.19±0.45) mol/L],the differences were statistically significant(P 0.05 or P 0.01);ROS concentration of cell cultures in ginsenoside CK low level group [(1.78±0.14) mol/L],middle level group [(1.56±0.23) mol/L] and high level group [(1.13±0.09) mol/L] were all lower than those in LPS group [(2.57±0.13) mol/L],the differences were statistically significant(P 0.05 or P 0.01).Conclusion Ginsenoside CK has anti-inflammatory and neuroprotective effects,hope to become the drugs for prevention of cerebral ischemia and other inflammatory diseases.Inhibition the microglial activation may be the mech anism of action.

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Objective To observe the anti-inflammatory and neuroprotective effects of ginsenoside CK and to investi gate the mechanism of action.Methods ①Lipopolysaccharide(LPS) induced murine sepsis model was copied,the ef fects of ginsenoside CK on brain microglia changes,tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were observed.②Rat models of cerebral ischemia reperfusion injury was duplicated,the effects of ginsenoside CK on the infarct volume percentage and microglial cell change were observed.③ Microglial cells were primary cultured to observe the effects of ginsenoside CK on LPS induced cell activation and culture medium of nitric oxide(NO) content and intracellular reactive oxygen species(ROS) content changes.Results ①TNF-α and IL-1β in model control group [(198.38±12.84) mg/L,(845.15±41.97) ng/L] were higher than those in normal control group [(106.71 ±11.21) mg/L,(477.46±49.76) ng/L],positive control group [(141.46±11.91) mg/L,(690.94±54.71) ng/L] and ginsenoside CK low level group [(157.23 ±12.25) mg/L,(726.04 ±64.29) ng/L],middle level group [(136.58 ±13.17) mg/L,(651.88 ±55.65) ng/L],high level group [(121.33±12.09) mg/L(577.36±51.86) ng/L],the differences were statistically significant(P 0.05 or P 0.01).②Lectin positive cell numbers of focal cerebral ischemia-reperfusion injury in rats in ginsenoside CK low level group [(30±7) numbers/500 μm2],middle level group [(20±5) numbers/500 μm2] and high level group [(13±4) numbers/500 μm2] were all lower than those in model group [(46±11) numbers/500 μm2],the differences were statistically significant(P 0.05 or P 0.01).Compared with model group,the infarct volume percentages in the ginsenoside CK low level group,middle level group,high level group significantly reduced(P 0.05 or P 0.01).③NO concentration of cell cultures in ginsenoside CK low level group [(18.16 ±0.59) mol/L],middle level group [(12.43 ±0.52) mol/ L] and high level group [(6.17±0.34) mol/L] were all lower than those in LPS group [(23.19±0.45) mol/L],the differences were statistically significant(P 0.05 or P 0.01);ROS concentration of cell cultures in ginsenoside CK low level group [(1.78±0.14) mol/L],middle level group [(1.56±0.23) mol/L] and high level group [(1.13±0.09) mol/L] were all lower than those in LPS group [(2.57±0.13) mol/L],the differences were statistically significant(P 0.05 or P 0.01).Conclusion Ginsenoside CK has anti-inflammatory and neuroprotective effects,hope to become the drugs for prevention of cerebral ischemia and other inflammatory diseases.Inhibition the microglial activation may be the mech anism of action.

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Available abstract

Objective To observe the anti-inflammatory and neuroprotective effects of ginsenoside CK and to investi gate the mechanism of action.Methods ①Lipopolysaccharide(LPS) induced murine sepsis model was copied,the ef fects of ginsenoside CK on brain microglia changes,tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were observed.②Rat models of cerebral ischemia reperfusion injury was duplicated,the effects of ginsenoside CK on the infarct volume percentage and microglial cell change were observed.③ Microglial cells were primary cultured to observe the effects of ginsenoside CK on LPS induced cell activation and culture medium of nitric oxide(NO) content and intracellular reactive oxygen species(ROS) content changes.Results ①TNF-α and IL-1β in model control group [(198.38±12.84) mg/L,(845.15±41.97) ng/L] were higher than those in normal control group [(106.71 ±11.21) mg/L,(477.46±49.76) ng/L],positive control group [(141.46±11.91) mg/L,(690.94±54.71) ng/L] and ginsenoside CK low level group [(157.23 ±12.25) mg/L,(726.04 ±64.29) ng/L],middle level group [(136.58 ±13.17) mg/L,(651.88 ±55.65) ng/L],high level group [(121.33±12.09) mg/L(577.36±51.86) ng/L],the differences were statistically significant(P 0.05 or P 0.01).②Lectin positive cell numbers of focal cerebral ischemia-reperfusion injury in rats in ginsenoside CK low level group [(30±7) numbers/500 μm2],middle level group [(20±5) numbers/500 μm2] and high level group [(13±4) numbers/500 μm2] were all lower than those in model group [(46±11) numbers/500 μm2],the differences were statistically significant(P 0.05 or P 0.01).Compared with model group,the infarct volume percentages in the ginsenoside CK low level group,middle level group,high level group significantly reduced(P 0.05 or P 0.01).③NO concentration of cell cultures in ginsenoside CK low level group [(18.16 ±0.59) mol/L],middle level group [(12.43 ±0.52) mol/ L] and high level group [(6.17±0.34) mol/L] were all lower than those in LPS group [(23.19±0.45) mol/L],the differences were statistically significant(P 0.05 or P 0.01);ROS concentration of cell cultures in ginsenoside CK low level group [(1.78±0.14) mol/L],middle level group [(1.56±0.23) mol/L] and high level group [(1.13±0.09) mol/L] were all lower than those in LPS group [(2.57±0.13) mol/L],the differences were statistically significant(P 0.05 or P 0.01).Conclusion Ginsenoside CK has anti-inflammatory and neuroprotective effects,hope to become the drugs for prevention of cerebral ischemia and other inflammatory diseases.Inhibition the microglial activation may be the mech anism of action.

Key concepts: Medicine, Neuroprotection, Nitric oxide, Lipopolysaccharide, Tumor necrosis factor alpha, Ginsenoside, Pharmacology, Ischemia

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