Investigating the beneficial effect of aliskiren in attenuating neuropathic pain in diabetic Sprague‐Dawley rats

Alkhudhayri, Shouq; Sajini, Rania; Alharbi, Bashayer; Qabbani, Jumana; Alhindi, Yosra; Fairaq, Arwa; Yousef, Amel M.

doi:10.1002/edm2.209

Cited by 7 publications

(4 citation statements)

References 26 publications

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“…In our clinical study, the number of T2DM patients receiving aliskiren, a renin inhibitor, was quite limited, so that the effect of aliskiren on DPN development could not be analyzed. Nonetheless, it is to be noted that an animal study demonstrated the beneficial effect of aliskiren in attenuating DPN in streptozotocin-induced diabetic rats 46 . Considering the significant impact of β-blockers on DPN development in the clinical study (see Table 2 ), the peripheral β-adrenoceptor/renin/Ang/AT 1 receptor system appears to participate in DPN development accompanying T2DM, and may serve as therapeutic targets for DPN.…”

Section: Discussionmentioning

confidence: 99%

Clinical and preclinical evidence that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers prevent diabetic peripheral neuropathy

Iwane,

Nemoto,

Miyamoto

et al. 2024

Sci Rep

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Given possible involvement of the central and peripheral angiotensin system in pain processing, we conducted clinical and preclinical studies to test whether pharmacological inhibition of the angiotensin system would prevent diabetic peripheral neuropathy (DPN) accompanying type 2 diabetes mellitus (T2DM). In the preclinical study, the nociceptive sensitivity was determined in leptin-deficient ob/ob mice, a T2DM model. A clinical retrospective cohort study was conducted, using the medical records of T2DM patients receiving antihypertensives at three hospitals for nearly a decade. In the ob/ob mice, daily treatment with perindopril, an angiotensin-converting enzyme inhibitor (ACEI), or telmisartan, an angiotensin receptor blocker (ARB), but not amlodipine, an L-type calcium channel blocker (CaB), significantly inhibited DPN development without affecting the hyperglycemia. In the clinical study, the enrolled 7464 patients were divided into three groups receiving ACEIs, ARBs and the others (non-ACEI, non-ARB antihypertensives). Bonferroni’s test indicated significantly later DPN development in the ARB and ACEI groups than the others group. The multivariate Cox proportional analysis detected significant negative association of the prescription of ACEIs or ARBs and β-blockers, but not CaBs or diuretics, with DPN development. Thus, our study suggests that pharmacological inhibition of the angiotensin system is beneficial to prevent DPN accompanying T2DM.

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Section: Discussionmentioning

confidence: 99%

Clinical and preclinical evidence that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers prevent diabetic peripheral neuropathy

Iwane,

Nemoto,

Miyamoto

et al. 2024

Sci Rep

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“…Considerable preclinical data has shown that RAS inhibitors, such as angiotensinconverting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB), exert a neuroprotective effect in various murine models of peripheral neuropathy [4,5], such as traumatic [6][7][8], diabetic [9][10][11] and toxin-induced neuropathies [12]. A beneficial effect of ramipril, an ACEi, was demonstrated in animal models of chronic constriction injury, streptozotocin-induced diabetes, and oxaliplatin-induced acute pain syndrome [6,11,13]. Recently, Kim et al reported that preventive or curative treatment with losartan, an ARB, delayed the onset of mechanical allodynia induced by PTX in rats [14].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of Ramipril Is Mediated by AT2 in a Mouse MODEL of Paclitaxel-Induced Peripheral Neuropathy

et al. 2022

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Paclitaxel (PTX)-induced peripheral neuropathy (PIPN) induces numerous symptoms affecting patient quality of life, leading to decreased doses or even to cessation of anticancer therapy. Previous studies have reported that a widely used drug, ramipril, improves neuroprotection in several rodent models of peripheral neuropathy. The protective role of the angiotensin II type 2 receptor (AT2) in the central and peripheral nervous systems is well-established. Here, we evaluate the effects of ramipril in the prevention of PIPN and the involvement of AT2 in this effect. Paclitaxel was administered in wild type or AT2-deficient mice on alternate days for 8 days, at a cumulative dose of 8 mg/kg (2 mg/kg per injection). Ramipril, PD123319 (an AT2 antagonist), or a combination of both were administered one day before PTX administration, and daily for the next twenty days. PTX-administered mice developed mechanical allodynia and showed a loss of sensory nerve fibers. Ramipril prevented the functional and morphological alterations in PTX mice. The preventive effect of ramipril against tactile allodynia was completely absent in AT2-deficient mice and was counteracted by PD123319 administration in wild type mice. Our work highlights the potential of ramipril as a novel preventive treatment for PIPN, and points to the involvement of AT2 in the neuroprotective role of ramipril in PIPN.

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“…The ineffectiveness of medical interventions arises partly due to the poorly understood molecular mechanism of neuropathic pain. Both peripheral and central sensitization are known to be implicated in the pathogenesis of neuropathic pain 23‐25 . Whereas the anomalous excitability of the primary sensory neurons during peripheral sensitization may be due to maladaptive changes in the gene transcription and translation of enzymes, receptors, and voltage‐dependent ion channels in the dorsal root ganglion, neuroinflammation caused by pathological microglia activation takes a major part in the process of central sensitization 26‐29 .…”

Section: Introductionmentioning

confidence: 99%

“…Both peripheral and central sensitization are known to be implicated in the pathogenesis of neuropathic pain. 23 , 24 , 25 Whereas the anomalous excitability of the primary sensory neurons during peripheral sensitization may be due to maladaptive changes in the gene transcription and translation of enzymes, receptors, and voltage‐dependent ion channels in the dorsal root ganglion, neuroinflammation caused by pathological microglia activation takes a major part in the process of central sensitization. 26 , 27 , 28 , 29 However, how the deranged molecular pathways underlying peripheral and central sensitization could be targeted therapeutically is still an active area of investigation.…”

Section: Introductionmentioning

confidence: 99%

Emerging roles of circular RNAs in neuropathic pain

Sun

et al. 2021

Cell Proliferation

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Neuropathic pain is a major type of chronic pain caused by the disease or injury of the somatosensory nervous system. It afflicts about 10% of the general population with a significant proportion of patients’ refractory to conventional medical treatment. This highlights the importance of a better understanding of the molecular pathogenesis of neuropathic pain so as to drive the development of novel mechanism‐driven therapy. Circular RNAs (circRNAs) are a type of non‐coding, regulatory RNAs that exhibit tissue‐ and disease‐specific expression. An increasing number of studies reported that circRNAs may play pivotal roles in the development of neuropathic pain. In this review, we first summarize circRNA expression profiling studies on neuropathic pain. We also highlight the molecular mechanisms of specific circRNAs (circHIPK3, circAnks1a, ciRS‐7, cZRANB1, circZNF609 and circ_0005075) that play key functional roles in the pathogenesis of neuropathic pain and discuss their potential diagnostic, prognostic, and therapeutic utilization in the clinical management of neuropathic pain.

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Investigating the beneficial effect of aliskiren in attenuating neuropathic pain in diabetic Sprague‐Dawley rats

Cited by 7 publications

References 26 publications

Clinical and preclinical evidence that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers prevent diabetic peripheral neuropathy

Clinical and preclinical evidence that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers prevent diabetic peripheral neuropathy

Neuroprotective Effect of Ramipril Is Mediated by AT2 in a Mouse MODEL of Paclitaxel-Induced Peripheral Neuropathy

Emerging roles of circular RNAs in neuropathic pain

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