Kisspeptin-10 protects against HIV-1 Tat-induced blood-brain barrier dysfunction and neuroinflammation via RhoA/ROCK pathway: Implications for HAND therapy.

Cheng C, Xiong D, Zheng F, Wang T, Li W

Neurotoxicology23 Jul 2025

PMID40712838DOI10.1016/j.neuro.2025.07.008PepBankPUB-40712838

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 study14

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 pretreatment attenuated the Tat-induced rise in cortical malondialdehyde.
In plain wordsIn mice, Kp-10 reduced the rise in an oxidative stress marker (MDA) in the brain caused by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
DecreaseMalondialdehyde (MDA) in cortical tissue
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
HIV-1 Tat increased oxidative stress in the cortical tissue of mice, as evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) activity, glutathione peroxidase (GSH-Px) activity, and total antioxidant capacity (T-AOC). These effects were attenuated by Kp-10 administration.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283801
02AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 pretreatment attenuated the Tat-induced fall in cortical catalase activity.
In plain wordsIn mice, Kp-10 reduced the fall in an antioxidant enzyme (catalase) in the brain caused by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
IncreaseCatalase activity in cortical tissue
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
HIV-1 Tat increased oxidative stress in the cortical tissue of mice, as evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) activity, glutathione peroxidase (GSH-Px) activity, and total antioxidant capacity (T-AOC). These effects were attenuated by Kp-10 administration.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283802
03AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 pretreatment attenuated the Tat-induced fall in cortical GSH-Px activity.
In plain wordsIn mice, Kp-10 reduced the fall in an antioxidant enzyme (GSH-Px) in the brain caused by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
IncreaseGlutathione peroxidase activity in cortical tissue
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
HIV-1 Tat increased oxidative stress in the cortical tissue of mice, as evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) activity, glutathione peroxidase (GSH-Px) activity, and total antioxidant capacity (T-AOC). These effects were attenuated by Kp-10 administration.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283803
04AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 pretreatment attenuated the Tat-induced fall in cortical total antioxidant capacity (T-AOC).
In plain wordsIn mice, Kp-10 reduced the fall in total antioxidant capacity in the brain caused by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
IncreaseTotal antioxidant capacity in cortical tissue
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
HIV-1 Tat increased oxidative stress in the cortical tissue of mice, as evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) activity, glutathione peroxidase (GSH-Px) activity, and total antioxidant capacity (T-AOC). These effects were attenuated by Kp-10 administration.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283804
05AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 suppressed the expression of interleukin-6.
In plain wordsIn mice, Kp-10 lowered the inflammatory signal IL-6 raised by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
DecreaseIL-6 expression
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Additionally, Kp-10 suppressed the expression of pro-inflammatory cytokines, including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α), in response to HIV-1 Tat.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283805
06AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 suppressed the expression of monocyte chemoattractant protein-1.
In plain wordsIn mice, Kp-10 lowered the inflammatory signal MCP-1 raised by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
DecreaseMCP-1 expression
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Additionally, Kp-10 suppressed the expression of pro-inflammatory cytokines, including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α), in response to HIV-1 Tat.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283806
07AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 suppressed the expression of tumor necrosis factor-alpha.
In plain wordsIn mice, Kp-10 lowered the inflammatory signal TNF-alpha raised by HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
DecreaseTNF-alpha expression
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Additionally, Kp-10 suppressed the expression of pro-inflammatory cytokines, including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α), in response to HIV-1 Tat.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283807
08AnimalAnimal study (in vivo)Efficacy outcome
In mice given HIV-1 Tat, Kp-10 mitigated blood-brain barrier dysfunction.
In plain wordsIn mice, Kp-10 reduced the damage that HIV-1 Tat did to the blood-brain barrier.
Peptide
Kisspeptin-10
Outcome
DecreaseHIV-1 Tat-induced BBB dysfunction
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Notably, Kp-10 mitigated HIV-1 Tat-induced BBB dysfunction by upregulating Claudin-5 expression in the cortical tissue of mice.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283808
09AnimalAnimal study (in vivo)Mechanism
In mice given HIV-1 Tat, Kp-10 upregulated Claudin-5 expression in the cortex.
In plain wordsIn mice, Kp-10 raised levels of Claudin-5, a barrier protein, in the brain.
Peptide
Kisspeptin-10
Outcome
IncreaseClaudin-5 expression in cortical tissue
Study
mousen: not reported in source
HIV-1 Tat-induced oxidative stress and BBB dysfunction
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
50 nmol/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Notably, Kp-10 mitigated HIV-1 Tat-induced BBB dysfunction by upregulating Claudin-5 expression in the cortical tissue of mice.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg).
Report a problemFND-4071283809
10LabIn vitro (cells)Efficacy outcome
In bEnd.3 cells, Kp-10 prevented the HIV-1 Tat-induced increase in trans-endothelial permeability.
In plain wordsIn cells, Kp-10 prevented HIV-1 Tat from making a layer of brain blood-vessel cells leakier.
Peptide
Kisspeptin-10
Outcome
DecreaseTrans-endothelial permeability
Study
n: not reported in source
bEnd.3 endothelial cells treated with HIV-1 Tat
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Our results demonstrated that Kp-10 prevented HIV-1 Tat-induced increases in trans-endothelial permeability and reductions in transepithelial electrical resistance (TEER) by upregulating Claudin-5 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed.
Report a problemFND-4071283810
11LabIn vitro (cells)Efficacy outcome
In bEnd.3 cells, Kp-10 prevented the HIV-1 Tat-induced reduction in TEER.
In plain wordsIn cells, Kp-10 prevented HIV-1 Tat from lowering the electrical resistance of a brain blood-vessel cell layer.
Peptide
Kisspeptin-10
Outcome
IncreaseTransepithelial electrical resistance (TEER)
Study
n: not reported in source
bEnd.3 endothelial cells treated with HIV-1 Tat
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Our results demonstrated that Kp-10 prevented HIV-1 Tat-induced increases in trans-endothelial permeability and reductions in transepithelial electrical resistance (TEER) by upregulating Claudin-5 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed.
Report a problemFND-4071283811
12LabIn vitro (cells)Mechanism
In bEnd.3 cells, Kp-10 upregulated Claudin-5 expression, which prevented the Tat-induced permeability changes.
In plain wordsIn cells, Kp-10 raised a barrier protein, Claudin-5, in the presence of HIV-1 Tat.
Peptide
Kisspeptin-10
Outcome
IncreaseClaudin-5 expression in bEnd.3 cells
Study
n: not reported in source
bEnd.3 endothelial cells treated with HIV-1 Tat
Comparator
HIV-1 Tat alone
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Our results demonstrated that Kp-10 prevented HIV-1 Tat-induced increases in trans-endothelial permeability and reductions in transepithelial electrical resistance (TEER) by upregulating Claudin-5 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed.
Report a problemFND-4071283812
13LabIn vitro (cells)Mechanism
In bEnd.3 cells, Kp-10 inhibited activation of the RhoA/ROCK signaling pathway.
In plain wordsIn cells, Kp-10 switched off a signaling pathway (RhoA/ROCK) that HIV-1 Tat activates.
Peptide
Kisspeptin-10
Outcome
DecreaseRhoA/ROCK signaling activation
Study
n: not reported in source
bEnd.3 endothelial cells treated with HIV-1 Tat
Comparator
HIV-1 Tat alone
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, Kp-10 inhibited the activation of the RhoA/Rho-associated protein kinase (RhoA/ROCK) signaling pathway in bEnd.3 cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed.
Report a problemFND-4071283813
14LabIn vitro (cells)Mechanism
In bEnd.3 cells, overexpression of the RhoA-GTP Q63L mutant abolished the protective effects of Kp-10.
In plain wordsIn cells, switching on the RhoA pathway removed the protective effects of Kp-10, suggesting that Kp-10 works through RhoA/ROCK.
Peptide
Kisspeptin-10
Outcome
Not applicableProtective effect of Kp-10 with RhoA-GTP Q63L overexpression
Study
n: not reported in source
bEnd.3 endothelial cells treated with HIV-1 Tat
Comparator
Kp-10 without RhoA-GTP Q63L overexpression
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Overexpression of the RhoA-GTP Q63L mutant abolished the protective effects of Kp-10, suggesting that these effects are mediated through the RhoA/ROCK axis.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed.
Report a problemFND-4071283814

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

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Keywords

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