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	<front>
		<journal-meta>
			<journal-title-group>
				<journal-title>Zaporozhye Medical Journal</journal-title>
			</journal-title-group>
			<issn pub-type="epub">2310-1210</issn>
			<issn pub-type="ppub">2306-4145</issn>
			<publisher>
				<publisher-name>Zaporizhzhia State Medical and Pharmaceutical University</publisher-name>
			</publisher>
		</journal-meta>
		<article-meta>
			<article-id pub-id-type="doi">10.14739/2310-1210.2026.3.352377</article-id>
			<title-group>
				<article-title>Early neuroprotection: effects on p53 and annexin A5 protein expression in the basal magnocellular nucleus of rats with colchicine-induced injury</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3413-945X</contrib-id>
					<name>
						<name>M. V.</name>
						<given-names>Danukalo</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"/>
				</contrib>
			</contrib-group>
			<aff id="aff1">Zaporizhzhia State Medical and Pharmaceutical University</aff>
			<author-notes>
				<fn><p>Corresponding author Maksym Danukalo. E-mail: <email>danukalo.m.v@zsmu.edu.ua</email></p></fn>
			</author-notes>
			<pub-date pub-type="epub">
				<day>11</day>
				<month>06</month>
				<year>2026</year>
			</pub-date>
			<volume>28</volume>
			<issue>3</issue>
			<fpage>236</fpage>
			<lpage>244</lpage>
			<content-language>uk</content-language>
			<abstract>
				<p><bold>Aim.</bold> To determine the expression patterns of p53 and annexin A5 in the cells of the basal magnocellular nucleus (BMN) of the rat brain following early neuroprotective intervention with citicoline, thiocetam, and recombinant HSF-1 in a rat model of colchicine-induced neurodegeneration.</p>
				<p><bold>Materials and methods.</bold> The study involved 50 male Wistar rats divided into five groups (n = 10 each). Group 1 (control) received an intracerebroventricular (ICV) injection of 0.9 % NaCl solution. Animals in groups 2–5 received ICV colchicine. Group 2 served as the positive control (untreated pathology model). Groups 3–5 received citicoline, thiocetam, and HSF-1, respectively, for 14 consecutive days beginning the day after surgery. Subsequently, all rats were euthanized under thiopental sodium anesthesia, and the brains were harvested for histochemical and immunofluorescent analyses.</p>
				<p><bold>Results.</bold> ICV colchicine caused loss of the neuronal component and an increase in glial cell number in the BMN. A two-week course of neuroprotective correction prevented these changes. Colchicine-induced neurodegeneration was also associated with an elevated number of p53- and Annexin A5-immunopositive cells in the BMN. Notably, administration of citicoline and HSF-1 resulted in a further pronounced increase in p53-positive neurons (by 60–70 % relative to the pathology group), whereas thiocetam caused a significantly increased number of annexin A5-immunopositive cells. Concurrently, all types of pathogenetic correction normalized the Corrected Total Cell Fluorescence (CTCF) of annexin A5+ cells to control levels.</p>
				<p><bold>Conclusions.</bold> In the BMN of experimental animals on day 14 post-ICV colchicine injection, a decrease in neuronal density and an increase in glial density were observed compared to sham-operated rats. In contrast, in the groups receiving early administration of citicoline, thiocetam, or recombinant HSF-1, neuronal and glial density parameters remained at levels comparable to control animals. The highest CTCF values for annexin A5-positive cells were recorded in the colchicine group compared to both sham-operated and correction groups, with no statistically significant differences among the latter. At the same time, p53 CTCF values in the BMN across all experimental groups showed no statistically significant differences compared to the control or each other. While the total counts of p53- and annexin A5-positive cells in the colchicine group significantly exceeded those in sham-operated animals, this parameter in the correction groups varied according to the specific pharmacological agent used.</p>
			</abstract>
			<kwd-group kwd-group-type="author">
				<kwd>neuroprotection</kwd>
				<kwd>neurodegeneration</kwd>
				<kwd>apoptosis</kwd>
				<kwd>p53</kwd>
				<kwd>Annexin A5</kwd>
				<kwd>brain</kwd>
				<kwd>neurons</kwd>
				<kwd>citicoline</kwd>
				<kwd>thiocetam</kwd>
				<kwd>HSF-1</kwd>
			</kwd-group>
			<self-uri content_type="abstract">https://zmj.zsmu.edu.ua/article/view/352377</self-uri>
			<self-uri content_type="pdf">https://zmj.zsmu.edu.ua/article/download/352377/349963</self-uri>
		</article-meta>
	</front>
</article>
