Evidence map›Paper›PMID 36609633›Full record

ArticleMolecular and cellular biochemistry2023

Beneficial effects of buspirone in endothelin-1 induced stroke cachexia in rats.

Darshak Shah, Mit Joshi, Jigna Shah, Bhoomika M Patel

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Article in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Darshak ShahInstitute of Pharmacy, Nirma University, Ahmedabad, India.
Mit JoshiInstitute of Pharmacy, Nirma University, Ahmedabad, India.
Jigna ShahInstitute of Pharmacy, Nirma University, Ahmedabad, India.
Bhoomika M PatelNational Forensic Sciences University, Sector 9, Gandhinagar, Gujarat, 382007, India. drbhoomikampatel@gmail.com.ORCID http://orcid.org/0000-0003-0594-5452
Nirma University · INNational Forensic Sciences University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke cachexia is associated with prolonged inflammation, muscle loss, poor prognosis, and early death of stroke patients. No particular treatment is available to cure the symptoms or disease. The present study aimed to evaluate the effect of a 5-HT1a agonist, buspirone on stroke cachexia. Wistar rats were injected with endothelin-1 to the bregma region of the brain to induce ischemic stroke followed by induction of cachexia after 4 days. Treatment with buspirone (3 mg/kg p.o) was given for 4 weeks after confirmation of cachexia in animals. Disease control animals exhibited decrease in wire hanging time and increase in foot fault numbers compared to normal animals. Disease control animals also showed weight loss, decrease in food intake, increased serum glucose and lipid profile along with high serum levels of inflammatory cytokines-TNF-α, IL-6 and decrease in weight of skeletal muscle and adipose tissues. Treatment with buspirone improves behavioural parameters along with increases food intake and body weight, decreased inflammatory cytokines IL-6 and TNF-α and serum glucose levels with increase in lipid profile. Buspirone also increased the weight of adipose tissue and maintain the skeletal muscle architecture and function as depicted in histopathological studies. Our study suggests that buspirone produces beneficial role in stroke cachexia by increasing body weight, food intake and adipose tissue depots by activating on 5-HT receptors. Buspirone decreases inflammatory markers in stroke cachexia although mechanism behind it was not fully understood. Buspirone decreases circulating blood glucose by stimulating glucose uptake in skeletal muscle via 5-HT receptors and maintained lipid profile. Buspirone was found to be effective in ameliorating cachectic conditions in stroke.

Indexed as

CachexiaStrokeAnimalsBuspironeCytokinesEndothelin-1GlucoseInterleukin-6LipidsMuscle, SkeletalRatsRats, WistarTumor Necrosis Factor-alphaBuspironeCytokinesEndothelin-1GlucoseInterleukin-6LipidsTumor Necrosis Factor-alpha5-HTA1 receptor agonistIschemic strokeMuscle wastingStroke cachexia

Identifiers

PMID36609633
OpenAlexW4313703976

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.