Study on the protective effect of OM-MSCs on Golgi apparatus after intracerebral hemorrhage in Sprague-Dawley rats.

Introduction: The present study aimed to assess alterations in apoptosis rate, Golgi morphology and GOLPH3 expression following intracerebral hemorrhage (ICH) both before and after intervention with OM-MSCs. The objective was to investigate the impact of ICH on Golgi apparatus (GA) stress and to explore the potential protective effects of OM-MSCs on GA following ICH.

Material And Methods: A total of 54 Sprague-Dawley rats were allocated into three experimental groups: sham operation group, ICH group and OM-MSCs group. ICH models were established by collagenase method while OM-MSCs were cultured in vitro. In OM-MSCs intervention group, one million OM-MSCs were stereotactically injected into unilateral striatum of rats 48 hours after ICH modeling while other two groups received an equivalent volume of PBS. Brain tissues were collected at 1 day, 3 day and 7 day post intervention and subsequently assessed for cellular apoptosis, morphological change of GA and expression of GOLPH3. The obtained data were subjected to statistical analysis by SPSS 21.0.

Results: 1. Apoptosis rate in the 1 d and 3 d ICH groups was significantly higher compared to sham operation group (P < 0.05), but significantly lower compared to OM-MSCs intervention group (P < 0.05). 2. While no noticeable morphological changes were observed in sham operation group, GA in ICH group exhibited a significant increase fragmentation. After OM-MSCs intervention, the fragmentation of GA decreased significantly. 3. On 3 d, expression of GOLPH3 in ICH group was significantly higher than that in sham operation group (P < 0.05) but significantly lower than that of OM-MSCs intervention group (P < 0.05).

Conclusions: The rate of apoptosis, fragmentation of GA, and expression of GOLPH3 exhibited significant increases following ICH in SD rats. Conversely, all of these factors demonstrated significant decreases subsequent to early intervention with OM-MSCs, thereby exerting neuroprotective effects.