Use of salidroside in a lipopolysaccharide-induced periventricular leukomalacia model


Article PDF :

Veiw Full Text PDF

Article type :

Original Article

Author :

Mustafa Dilek, Gokce Kaya Dincel, Ayhan Cetinkaya, Mervan Bekdas, Nimet Kabakus

Volume :

1

Issue :

4

Abstract :

Aim: Research into the different treatment methods based on the intrauterine lipopolysaccharide (LPS)-induced periventricular leukomalacia (PVL) model, as one of the main causes of morbidity in preterm infants still continues to be relevant. The present study investigates the effect on PVL of salidroside obtained from Rhodiola Rosea (golden root, orpin rose), which is a plant with known for its medicinal qualities. Method: To develop an induced PVL model, a 500 microgram/kg dose of LPS (Escherichia coli, serotype 055:B5, Sigma) was applied to two pregnant rats intraperitoneally on day 18, day 19 and day 20 of gestation. One of the LPS applied rats was given 25 mg/kg salidroside (250 mg Rhodiola root extract capsules, which include 3 mg salidroside) by oral gavage (LPS+Salidroside), and a physiological saline solution was given to the control group. After delivery, 10 offspring of the LPS-applied mother, nine offspring of the LPS+Salidrosideapplied mother and seven offspring of the control mother were sacrificed on postnatal day 7 with ether anesthesia. The caspase enzyme located in apoptosis pathways of 10 percent neutral-buffered formalin fixed brain tissue was stained immunohistochemically, and apoptotic cells were counted. Results: No statistically significant difference was noted between the LPS+Salidroside group and the control group, while a statistically significant difference was noted between the LPS and LPS+Salidroside groups. It was observed that salidroside reduced LPS induced apoptosis. Conclusion: The intended experimental neuroprotective effect of salidroside usage was provided through the inhibition of apoptosis in a PVL-damaged brain.

Keyword :

Salidroside; lipopolysaccharide; periventricular leukomalacia; rat model; neuroprotection.
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