Kisspeptin-10 Preserves the Blood-Brain Barrier's Integrity Post-Stroke by Augmenting Claudin-10 Expression.

Li L, Guo Y, Zhao K

Clinical and experimental pharmacology & physiology1 Nov 2025

PMID41022671DOI10.1111/1440-1681.70079PepBankPUB-41022671

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

8 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with middle cerebral artery occlusion, Kp-10 administration alleviated neurological deficits.
In plain wordsIn mice with a stroke model, kisspeptin‑10 reduced signs of neurological damage.
Peptide
Kisspeptin-10
Outcome
DecreaseNeurological deficits (Longa score)
Study
mousen: not reported in source
MCAO model in C57BL/6 mice
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Subsequent administration of Kp-10 not only alleviated neurological deficits
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice, followed by Kp-10 administration.
Report a problemFND-4102267102
02AnimalAnimal study (in vivo)Efficacy outcome
In mice with middle cerebral artery occlusion, Kp-10 administration significantly mitigated blood-brain barrier dysfunction, with reduced 14C-sucrose leakage.
In plain wordsIn mice with a stroke model, kisspeptin‑10 reduced leakage across the blood-brain barrier.
Peptide
Kisspeptin-10
Outcome
DecreaseBlood-brain barrier permeability (14C-sucrose leakage)
Study
mousen: not reported in source
MCAO model in C57BL/6 mice
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
significantly mitigated blood-brain barrier (BBB) dysfunction following stroke induction, as evidenced by reduced 14C-sucrose leakage.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice, followed by Kp-10 administration.
Report a problemFND-4102267103
03AnimalAnimal study (in vivo)Mechanism
In mice with middle cerebral artery occlusion, Kp-10 treatment upregulated Claudin-10 expression in the post-stroke cortical region.
In plain wordsIn mice with a stroke model, kisspeptin‑10 raised Claudin-10, a protein that seals the blood-brain barrier.
Peptide
Kisspeptin-10
Outcome
IncreaseClaudin-10 expression in post-stroke cortex
Study
mousen: not reported in source
MCAO model in C57BL/6 mice
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, Kp-10 treatment led to an upregulation of Claudin-10 expression in the post-stroke cortical region.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice, followed by Kp-10 administration.
Report a problemFND-4102267104
04LabIn vitro (cells)Efficacy outcome
In human brain microvascular endothelial cells exposed to OGD/R, Kp-10 reduced endothelial permeability by enhancing Claudin-10 expression.
In plain wordsIn human brain blood-vessel cells in the lab, kisspeptin‑10 reduced leakiness under stroke-like conditions.
Peptide
Kisspeptin-10
Outcome
DecreaseEndothelial permeability after OGD/R
Study
humann: not reported in source
HBMVECs under oxygen-glucose deprivation/reoxygenation
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
We found that Kp-10 effectively reduced OGD/R-induced endothelial permeability by enhancing Claudin-10 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
Human brain microvascular endothelial cells (HBMVECs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemic conditions.
Report a problemFND-4102267105
05LabIn vitro (cells)Efficacy outcome
In human brain microvascular endothelial cells exposed to OGD/R, Kp-10 decreased mitochondrial reactive oxygen species levels.
In plain wordsIn human brain blood-vessel cells in the lab, kisspeptin‑10 lowered harmful reactive oxygen molecules in mitochondria.
Peptide
Kisspeptin-10
Outcome
DecreaseMitochondrial ROS levels
Study
humann: not reported in source
HBMVECs under oxygen-glucose deprivation/reoxygenation
Outcome group
Mitochondrial function · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Additionally, Kp-10 exhibited antioxidant capabilities by decreasing mitochondrial reactive oxygen species (ROS) levels, increasing superoxide dismutase (SOD) activity, and upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) expression.
1 context sentence(design, population, supporting numbers)
Summary · context
Human brain microvascular endothelial cells (HBMVECs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemic conditions.
Report a problemFND-4102267106
06LabIn vitro (cells)Mechanism
In human brain microvascular endothelial cells exposed to OGD/R, Kp-10 increased superoxide dismutase activity.
In plain wordsIn human brain blood-vessel cells in the lab, kisspeptin‑10 raised the activity of an antioxidant enzyme.
Peptide
Kisspeptin-10
Outcome
IncreaseSuperoxide dismutase activity
Study
humann: not reported in source
HBMVECs under oxygen-glucose deprivation/reoxygenation
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Additionally, Kp-10 exhibited antioxidant capabilities by decreasing mitochondrial reactive oxygen species (ROS) levels, increasing superoxide dismutase (SOD) activity, and upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) expression.
1 context sentence(design, population, supporting numbers)
Summary · context
Human brain microvascular endothelial cells (HBMVECs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemic conditions.
Report a problemFND-4102267107
07LabIn vitro (cells)Mechanism
In human brain microvascular endothelial cells exposed to OGD/R, Kp-10 upregulated Nrf2 expression.
In plain wordsIn human brain blood-vessel cells in the lab, kisspeptin‑10 raised Nrf2, a protein that controls antioxidant defence.
Peptide
Kisspeptin-10
Outcome
IncreaseNrf2 expression
Study
humann: not reported in source
HBMVECs under oxygen-glucose deprivation/reoxygenation
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Additionally, Kp-10 exhibited antioxidant capabilities by decreasing mitochondrial reactive oxygen species (ROS) levels, increasing superoxide dismutase (SOD) activity, and upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) expression.
1 context sentence(design, population, supporting numbers)
Summary · context
Human brain microvascular endothelial cells (HBMVECs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemic conditions.
Report a problemFND-4102267108
08LabIn vitro (cells)Mechanism
In human brain microvascular endothelial cells, Nrf2 knockdown abolished the protective effects of Kp-10 on endothelial permeability and Claudin-10 expression.
In plain wordsIn human brain blood-vessel cells in the lab, kisspeptin‑10 lost its protective effect when Nrf2 was knocked down.
Peptide
Kisspeptin-10
Outcome
Not applicableEffect of Nrf2 knockdown on Kp-10 protection
Study
humann: not reported in source
HBMVECs with Nrf2 knockdown
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Notably, when Nrf2 was knocked down in HBMVECs, the protective effects of Kp-10 on endothelial permeability and Claudin-10 expression were abolished, indicating that the beneficial actions of Kp-10 are mediated through the Nrf2 pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
Nrf2 silencing was performed to validate its role in Kp-10-mediated protection.
Report a problemFND-4102267109

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

09AnimalEndogenous levelAnimal study (in vivo)Other
In mice with middle cerebral artery occlusion, Kp-10 expression in cortical tissue was significantly reduced.
In plain wordsIn mice with a stroke model, the body's own kisspeptin‑10 was lower in brain cortex tissue.
Peptide
Kisspeptin-10
Outcome
DecreaseKp-10 expression in cortical tissue after MCAO
Study
mousen: not reported in source
MCAO model in C57BL/6 mice
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Initially, we observed a significant reduction in Kp-10 expression within the cortical tissue of mice subjected to MCAO.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice, followed by Kp-10 administration.
This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4102267101

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
Version 1
9 Oct 2026, 03:04 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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