Department Of Pharmacology

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Author: search.filters.author.Singh, NirmalHas files: No

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    Exploring the ameliorative potential of Bacopa monnieri in acetic acid induced ulcerative colitis in mice
    (Taylor and Francis Ltd., 2023-07-10T00:00:00) Devi, Karam; Bali, Anjana; Bhatia, Pankaj; Singh, Nirmal; Jaggi, Amteshwar Singh
    The aim of the present study was to evaluate the role of Bacopa monnieri in acetic-acid-induced ulcerative colitis in mice. Acetic acid (3%v/v, in 0.9% saline) was infused intrarectally to induce ulceration in mice. Administration of acetic acid resulted in severe inflammation of the colon along with an increase in the myeloperoxidase (MPO) activity assessed on 7th day. Treatment with Bacopa monnieri extract (20 mg/kg and 40 mg/kg, p.o) and saponin-rich fraction (5 mg/kg and 10 mg/kg; p.o) for 7 days i.e. 2 days before and 5 days after acetic acid infusion, significantly attenuated the colonic inflammation in a dose-dependent manner. Furthermore, it also reduced the MPO levels and the disease activity score as compared to the control group. It may be concluded that Bacopa monnieri has the potential for ameliorating acetic-acid-induced colitis and its saponin-rich fraction may be responsible for this effect. � 2023 Informa UK Limited, trading as Taylor & Francis Group.
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    Ephrin B/EphB in neuropathic pain: Role and molecular mechanisms
    (John Wiley and Sons Inc, 2023-07-04T00:00:00) Kaur, Sahibpreet; Bali, Anjana; Singh, Nirmal; Jaggi, Amteshwar Singh
    Ephrins are protein ligands that act through the tyrosine kinase receptor family, Eph receptors. The role of ephrin/Eph in the critical processes involved in the development of the nervous system, including axon guidance and cell migration, has been well documented. Moreover, studies have shown an upregulation of ephrin B1/EphB1 and ephrin B2/EphB2 in neuropathic pain of different etiology. The activation of the ephrin B/EphB system in the dorsal root ganglion and dorsal horn of the spinal cord may be essential in initiating and maintaining neuropathic pain. Accordingly, it can be proposed that the pharmacological inhibitors of EphB receptors may be potentially employed to manage the manifestations of pain. One of the primary mechanisms involved in ephrin B/EphB-mediated synaptic plasticity includes phosphorylation and activation of NMDA receptors, which may be secondary to activation of different kinases, including MAP kinases (MAPK), protein kinase C (PKC), and Src family kinases (SFK). The other molecular mechanisms may include activation of inflammatory cytokines in the spinal cord, caspase-3, calpain-1, phosphoinositide 3-kinase (PI3K), protein kinase A (PKA), and cAMP Response Element-Binding Protein (CREB). The present review discusses the role and molecular mechanisms involved in ephrin B/EphB-mediated neuropathic pain of different etiology. � 2023 Soci�t� Fran�aise de Pharmacologie et de Th�rapeutique. Published by John Wiley & Sons Ltd.
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    Demystifying the dual role of the angiotensin system in neuropathic pain
    (Churchill Livingstone, 2022-05-26T00:00:00) Kaur, Sahibpreet; Bali, Anjana; Singh, Nirmal; Jaggi, Amteshwar Singh
    Neuropathic Pain is caused by damage to a nerve or disease of the somatosensory nervous system. Apart from the blood pressure regulating actions of angiotensin ligands, studies have shown that it also modulates neuropathic pain. In the animal models including surgical, chemotherapeutic, and retroviral-induced neuropathic pain, an increase in the levels of angiotensin II has been identified and it has been proposed that an increase in angiotensin II may participate in the induction of neuropathic pain. The pain-inducing actions of the angiotensin system are primarily due to the activation of AT1 and AT2 receptors, which trigger the diverse molecular mechanisms including the induction of neuroinflammation to initiate and maintain the state of neuropathic pain. On the other hand, the pain attenuating action of the angiotensin system has been attributed to decreasing in the levels of Ang(1�7), and Ang IV and an increase in the levels of bradykinin. Ang(1�7) may attenuate neuropathic pain via activation of the spinal Mas receptor. However, the detailed molecular mechanism involved in Ang(1�7) and Ang IV-mediated pain attenuating actions needs to be explored. The present review discusses the dual role of angiotensin ligands in neuropathic pain along with the possible mechanisms involved in inducing or attenuating the state of neuropathic pain. � 2022 Elsevier Ltd