Pulmonary inflammation, oxidative stress, and fibrosis in a mouse model of cholestasis: the potential protective properties of the dipeptide carnosine

Ommati, Mohammad Mehdi; Sabouri, Samira; Niknahad, Hossein; Arjmand, Abdollah; Alidaee, Sepideh; Mazloomi, Sahra; Najibi, Asma; Rezaei, Heresh; Ghiasvand, Alireza; Ahmadi, Parinaz; Nikoozadeh, Ahmad; Khodaei, Forouzan; Abdoli, Narges; Azarpira, Negar; Heidari, Reza

doi:10.1007/s00210-023-02391-y

Cited by 3 publications

(1 citation statement)

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“…2′,7′-dichlorofluorescein-diacetate (DCF-DA) was used as a fluorescent probe to assess ROS formation in the brain tissue. [55][56][57] For this purpose, 100 µL of tissue homogenate (in KCl 1.15% w-v, 4°C) was mixed with 900 µL of phosphate buffer and 10 μL of DCF-DA (Final concentration of 10 μM). [56] The mixture was incubated at 37°C (10 min, in the dark).…”

Section: Reactive Oxygen Species (Ros) Formation In the Brain Tissuementioning

confidence: 99%

Low‐dose ketamine improves animals' locomotor activity and decreases brain oxidative stress and inflammation in ammonia‐induced neurotoxicity

Ommati

Mobasheri

Niknahad

et al. 2023

J Biochem & Molecular Tox

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Ammonium ion (NH4+) is the major suspected molecule responsible for neurological complications of hepatic encephalopathy (HE). No specific pharmacological action for NH4+‐induced brain injury exists so far. Excitotoxicity is a well‐known phenomenon in the brain of hyperammonemic cases. The hyperactivation of the N‐Methyl‐ d‐aspartate (NMDA) receptors by agents such as glutamate, an NH4+ metabolite, could cause excitotoxicity. Excitotoxicity is connected with events such as oxidative stress and neuroinflammation. Hence, utilizing NMDA receptor antagonists could prevent neurological complications of NH4+ neurotoxicity. In the current study, C57BL6/J mice received acetaminophen (APAP; 800 mg/kg, i.p) to induce HE. Hyperammonemic animals were treated with ketamine (0.25, 0.5, and 1 mg/kg, s.c) as an NMDA receptor antagonist. Animals' brain and plasma levels of NH4+ were dramatically high, and animals' locomotor activities were disturbed. Moreover, several markers of oxidative stress were significantly increased in the brain. A significant increase in brain tissue levels of TNF‐α, IL‐6, and IL‐1β was also detected in hyperammonemic animals. It was found that ketamine significantly normalized animals' locomotor activity, improved biomarkers of oxidative stress, and decreased proinflammatory cytokines. The effects of ketamine on oxidative stress biomarkers and inflammation seem to play a key role in its neuroprotective mechanisms in the current study.

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