Caffeine improves bladder function in diabetic rats via a neuroprotective effect

Xue, Jun; Liu, Yadong; Zhang, Sichong; Ding, Liang; Shen, Baixin; Shao, Yunpeng; Wei, Zuoan

doi:10.3892/etm.2021.9932

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…Some studies suggest that caffeine may upregulate Bax expression or downregulate Bcl-2 expression, thereby promoting apoptosis in certain conditions [ 44 ]. Conversely, in other contexts, caffeine may exert neuroprotective effects by decreasing Bax expression or increasing Bcl-2 expression, thus inhibiting apoptosis and promoting cell survival [ 45 ]. The decrease in proapoptotic Bax levels and changes in Bcl-2 and caspase-3 levels across treatments underscore the complex interplay between caffeine, melatonin, and VA on the cellular survival pathways.…”

Section: Discussionmentioning

confidence: 99%

Impact of a Novel Valerian Extract on Sleep Quality, Relaxation, and GABA/Serotonin Receptor Activity in a Murine Model

Sahin,

Gencoglu,

Korkusuz

et al. 2024

Antioxidants

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Insomnia is a major global health issue, highlighting the need for treatments that are both effective and safe. Valerian extract, a traditional remedy for sleep problems, offers potential therapeutic options. This research examined the potential sleep-enhancing effects of VA (Valerian Pdr%2) in mice. The study evaluated sleep quality by comparing the impact of the VA extract against melatonin on brain activity, using electrocorticography (ECoG) to assess changes in brain waves. For this purpose, the study utilized two experimental models on BALB/c mice to explore the effects of caffeine-induced insomnia and pentobarbital-induced sleep. In the first model, 25 mice were assigned to five groups to test the effects of caffeine (caffeine, 7.5 mg/kg i.p) alone, caffeine with melatonin (2 mg/kg), or caffeine with different doses of valerian extract (100 or 300 mg/kg) given orally on brain activity, assessed via electrocorticography (ECoG) and further analyses on the receptor proteins and neurotransmitters. In the second model, a different set of 25 mice were divided into five groups to examine the impact of pentobarbital (42 mg/kg) alone, with melatonin, or with the valerian extract on sleep induction, observing the effects 45 min after administration. The study found that ECoG frequencies were lower in groups treated with melatonin and two doses of valerian extract (100 and 300 mg/kg), with 300 mg/kg showing the most significant effect in reducing frequencies compared to the caffeine control group, indicating enhanced sleep quality (p < 0.05). This was supported by increased levels of serotonin, melatonin, and dopamine and higher levels of certain brain receptors in the melatonin and valerian extract groups (p < 0.05). Modulatory efficacy for the apoptotic markers in the brain was also noted (p < 0.05). Additionally, melatonin and both doses of VA increased sleep duration and reduced sleep onset time compared to the pentobarbital control, which was particularly notable with high doses. In conclusion, the findings suggest that high doses (300 mg/kg) of valerian extract enhance both the quantity and quality of sleep through the GABAergic pathway and effectively increase sleep duration while reducing the time to fall asleep in a pentobarbital-induced sleep model in mice.

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Section: Discussionmentioning

confidence: 99%

Impact of a Novel Valerian Extract on Sleep Quality, Relaxation, and GABA/Serotonin Receptor Activity in a Murine Model

Sahin,

Gencoglu,

Korkusuz

et al. 2024

Antioxidants

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show abstract

“…Peak voiding pressure and voiding efficacy were significantly improved in rats treated with both doses of caffeine, yet the effect was greater at 10 mg/kg/day caffeine (Liu et al 2019 ). In a further study, female STZ-diabetic rats were treated with caffeine (10 mg/kg/day) for 16 weeks (Xue et al 2021 ). Caffeine treatment was found to improve voiding dysfunction by increasing expression of NGF, brain-derived neurotrophic factor, and calcitonin gene-related peptide in bladder tissue and by reducing apoptotic cells in dorsal root ganglion.…”

Section: Emerging Pathophysiology-based Treatments Of Lutd In Diabetesmentioning

confidence: 99%

“…Caffeine treatment was found to improve voiding dysfunction by increasing expression of NGF, brain-derived neurotrophic factor, and calcitonin gene-related peptide in bladder tissue and by reducing apoptotic cells in dorsal root ganglion. Reduced antiapoptotic protein Bcl-2 level in diabetic rats was markedly increased with caffeine treatment, and caffeine decreased the level of pro-apoptotic proteins such as Bax, cleaved caspase-3, and cleaved caspase-9 in dorsal root ganglion (Xue et al 2021 ).…”

Section: Emerging Pathophysiology-based Treatments Of Lutd In Diabetesmentioning

confidence: 99%

Established and emerging treatments for diabetes-associated lower urinary tract dysfunction

Erdogan

Liu

Arioglu‐Inan

et al. 2022

Naunyn-Schmiedeberg's Arch Pharmacol

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Dysfunction of the lower urinary tract (LUT) including urinary bladder and urethra (and prostate in men) is one of the most frequent complications of diabetes and can manifest as overactive bladder, underactive bladder, urinary incontinence, and as aggravated symptoms of benign prostate hyperplasia. We have performed a selective literature search to review existing evidence on efficacy of classic medications for the treatment of LUT dysfunction in diabetic patients and animals, i.e., α1-adrenoceptor and muscarinic receptor antagonists, β3-adrenoceptor agonists, and phosphodiesterase type 5 inhibitors. Generally, these agents appear to have comparable efficacy in patients and/or animals with and without diabetes. We also review effects of antidiabetic medications on LUT function. Such studies have largely been performed in animal models. In the streptozotocin-induced models of type 1 diabetes, insulin can prevent and reverse alterations of morphology, function, and gene expression patterns in bladder and prostate. Typical medications for the treatment of type 2 diabetes have been studied less often, and the reported findings are not yet sufficient to derive robust conclusions. Thereafter, we review animal studies with emerging medications perhaps targeting diabetes-associated LUT dysfunction. Data with myoinositol, daidzein, and with compounds that target oxidative stress, inflammation, Rac1, nerve growth factor, angiotensin II receptor, serotonin receptor, adenosine receptor, and soluble guanylyl cyclase are not conclusive yet, but some hold promise as potential treatments. Finally, we review nonpharmacological interventions in diabetic bladder dysfunction. These approaches are relatively new and give promising results in preclinical studies. In conclusion, the insulin data in rodent models of type 1 diabetes suggest that diabetes-associated LUT function can be mostly or partially reversed. However, we propose that considerable additional experimental and clinical studies are needed to target diabetes itself or pathophysiological changes induced by chronic hyperglycemia for the treatment of diabetic uropathy.

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“…Neurotrophic factors are cytokines that regulate the growth and development of the nervous system. Endogenous neurotrophic factors can inhibit neuronal apoptosis ( Xue et al, 2021 ), promote neuronal axon growth and regulate neuronal differentiation ( de León et al, 2021 ). Different neurotrophic factors play different roles, and these roles can be synergistic or even opposite.…”

Section: Introductionmentioning

confidence: 99%

The GDF11 Promotes Nerve Regeneration After Sciatic Nerve Injury in Adult Rats by Promoting Axon Growth and Inhibiting Neuronal Apoptosis

Lin

Shi

Min

et al. 2022

Front. Bioeng. Biotechnol.

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Introduction: Sciatic nerve injury is a common injury of the nervous system. Stem cell-based therapies, drug-based therapies and rehabilitation physiotherapy therapies are currently available, but their limited therapeutic efficacy limits their use. Here, we aimed to explore a novel lentiviral-based gene therapeutic strategy and to elaborate its mechanism.Materials and Methods: Recombinant GDF11 protein was used for the in vitro treatment of dorsal root ganglion (DRG) cells. Lentivirus was used to construct a vector system for the in vivo expression of GDF11. The nerve conduction function was detected using action-evoked potentials at different time periods, and the regulatory effect of nerves on target organs was detected by weighing the gastrocnemius muscle. Immunofluorescence of NF200 and S100 was used to show the regeneration of the sciatic nerve, and myelin and Nissl staining were performed to observe the pathological features of the tissue. Western was used to validate signaling pathways. The expression of related genes was observed by qPCR and Western blotting, and cell apoptosis was detected by flow cytometry.Result: GDF11 promotes the axonal growth of DRG cells and inhibits DGR cell apoptosis in vitro. GDF11 acts by activating the Smad pathway. GDF11 promotes the recovery of damaged sciatic nerve function in rats, the regeneration of damaged sciatic nerves in rats, and myelin regeneration of damaged sciatic nerves in rats. GDF11 also exerts a protective effect on neuronal cells in rats.Conclusion: Based on the present study, we conclude that GDF11 promotes axonal growth and inhibits DRG cell apoptosis in vitro through the Smad pathway, and lentivirus-mediated GDF11 overexpression in vivo can promote the recovery of sciatic nerves after transection by promoting axonal growth and inhibiting neuronal apoptosis in the spinal cord.

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Caffeine improves bladder function in diabetic rats via a neuroprotective effect

Cited by 8 publications

References 27 publications

Impact of a Novel Valerian Extract on Sleep Quality, Relaxation, and GABA/Serotonin Receptor Activity in a Murine Model

Impact of a Novel Valerian Extract on Sleep Quality, Relaxation, and GABA/Serotonin Receptor Activity in a Murine Model

Established and emerging treatments for diabetes-associated lower urinary tract dysfunction

The GDF11 Promotes Nerve Regeneration After Sciatic Nerve Injury in Adult Rats by Promoting Axon Growth and Inhibiting Neuronal Apoptosis

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