LIU Jian-dong, ZHAO Chun-ying, TONG Ji-ming. Antipyretic Effect and its Mechanism of Tatol Organic Acid from Fruit on LPS-induced Febris Response in Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(6): 154-157.
DOI:
LIU Jian-dong, ZHAO Chun-ying, TONG Ji-ming. Antipyretic Effect and its Mechanism of Tatol Organic Acid from Fruit on LPS-induced Febris Response in Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(6): 154-157. DOI: 10.11653/syfj2014060154.
Antipyretic Effect and its Mechanism of Tatol Organic Acid from Fruit on LPS-induced Febris Response in Rats
Objective: To investigate the antipryretic effects and its possible mechanism of total arganic acid of Thladiantha dubia fruit (TOATDF). Method: The rat fever model was established by injection of lipopolysaccharides (LPS) of 100 μg·kg-1 and then the model rats were randomly divided into five groups:TOATDF 300
150
75 mg·kg-1 groups
Asprin 150 mg·kg-1 group(positive control)
and model control group
at the same time
normal rats as the control group. All groups were ig given the same volume drugs or saline. After treatment temperature was measured once each hour for 6 times. The levels of prostaglandin E2(PGE2)
tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in serum and PGE2 in cerebrospinal fluid were measured by enzyme linked immunosorbant assay(ELISA). Result: At each time point
the average temperature in TOATD 300
150 mg·kg-1groups was lower than that in the model control group(P<0.05 or P<0.01)
in TOATDF 75 mg·kg-1group and asprin group
the average temperature was lower than that in the model control group 2-5 h and 1-5 h after treatment
respectively. The expression levels of PGE2
TNF-α and IL-β in serum and PGE2 in cerebrospinal fluid were significantly lower than that of model group (P<0.05 or P<0.01)
but higher than that of normal control group (P<0.05). Conclusion: TOATDF has significant antipyretic effect on LPS-induced febris response in rats and in a dose-dependent manner. Its mechanism may be related to inhibiting expression of PGE2
TNF-α and IL-β in serum and PGE2 in cerebrospinal fluid.