Karımkhan, Hadı

Profile Picture
Name Variants
Hadı Karımkhan
Hadı, Karımkhan
Karımkhan, H.
KARIMKHAN Hadı
Hadı KARIMKHAN
KARiMKHAN Hadi
Karımkhan Hadı
Karimkhan, Hadi
H., Karımkhan
Hadi KARiMKHAN
Karımkhan, Hadı
Karimkhan, H.
Hadi Karimkhan
Karimkhan Hadi
Karimkhani, Hadi
Karimkhani,H.
Job Title
Dr.Öğr.Üyesi
Email Address
hadi.karimkhani@okan.edu.tr
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID
Scholarly Output

4

Articles

3

Citation Count

0

Supervised Theses

0

Filters

2020 - 20244
Reset filters

Settings

Scholarly Output Search Results

Now showing 1 - 4 of 4
  • Thumbnail Image
    Book Part
    Citation Count: 0
    The role of leptin as a biochemical marker in health and disease
    (Nova Science Publishers, Inc., 2023) Karimkhani,H.; Tıbbi Biyokimya / Medical Biochemistry
    Leptin is a hormone primarily produced by adipose tissue (fat cells) and is critical in regulating energy balance and metabolism (Martinez-Sanchez 2020; Abella et al. 2017). It functions as a satiety signal, which means it tells your brain when you've had enough to eat and helps regulate your appetite (Gioldasi et al. 2019). In addition, leptin affects the immune system, controls reproduction, and reduces inflammation (Francisco et al. 2018; Maurya et al. 2018). In healthy individuals, leptin levels rise after eating, which helps to decrease appetite and increase energy expenditure. In people who are overweight or obese, however, leptin levels are often high, but their brains do not respond appropriately to the signal (Martinez-Sanchez 2020; Akeel Al-hussaniy, Hikmate Alburghaif, and Akeel Naji 2021). This condition is known as leptin resistance, and it can contribute to obesity, insulin resistance, and other metabolic disorders. Leptin deficiency is another condition that can lead to obesity and other health problems. People with congenital leptin deficiency have very low levels of leptin from birth, which leads to uncontrolled appetite and severe obesity. Treatment with synthetic leptin is effective in reducing appetite and promoting weight loss in these individuals (Yupanqui-Lozno et al. 2019). Leptin receptors are found on immune cells, and the hormone has been shown to influence the production and activity of inflammatory cytokines. Elevated leptin levels have been linked to rheumatoid arthritis and an increased risk of chronic inflammation and autoimmune diseases, including multiple sclerosis. Overall, leptin is a critical hormone that plays a central role in regulating energy balance, metabolism, and immune function. Research on the function of leptin in health and sickness is ongoing, and future findings may result in new treatments for various conditions (Abella et al. 2017; Cojocaru et al. 2013; Martinez-Sanchez 2020). © 2024 by Nova Science Publishers, Inc. All rights reserved.
  • Thumbnail Image
    Article
    Citation Count: 0
    The effect of calpain inhibitor-I on copper oxide nanoparticle-induced damage and cerebral ischemia-reperfusion in a rat model
    (Elsevier France-editions Scientifiques Medicales Elsevier, 2024) Karimkhani, Hadi; Shojaolsadati, Paria; Yigitbasi, Turkan; Kolbasi, Bircan; Emekli, Neslin; Tıbbi Biyokimya / Medical Biochemistry
    This study aimed to investigate the effects of the calpain inhibitor N-Acetyl-Leu-Leu-norleucinal (ALLN) on neuroapoptotic cell damage caused by Copper Oxide Nanoparticles (CuO-NP) and exacerbation of damage through brain ischemia/reperfusion (I/R) in a rat model. Male Wistar Albino rats (n=80) were divided into eight groups: Control, I/R, CuO-NP, CuO-NP+I/R, I/R+ALLN, CuO-NP+ALLN, CuO-NP+I/R+ALLN, and DMSO. Biochemical markers (MBP, S100B, NEFL, NSE, BCL-2, Cyt-C, Calpain, TNF-alpha, Caspase-3, MDA, and CAT) were measured in serum and brain tissue samples. Histological examinations (H&E staining), DNA fragmentation analysis (TUNEL) were performed, along with Caspase-3 assessment. The ALLN-treated groups exhibited significant improvements in biochemical markers and a remarkable reduction in apoptosis compared to the damaged groups (CuO-NP and I/R). H&E and Caspase-3 staining revealed damage-related morphological changes and reduced apoptosis in the ALLN-treated group. However, no differences were observed among the groups with TUNEL staining. The findings suggest that ALLN, as a calpain inhibitor, has potential implications for anti-apoptotic treatment, specifically in mitigating neuroapoptotic cell damage caused by CuO-NP and I/R.
  • Thumbnail Image
    Article
    Citation Count: 6
    Protective Effect of Boric Acid and Omega-3 on Myocardial Infarction in an Experimental Rat Model
    (Springernature, 2021) Karimkhani, Hadi; Ozkoc, Mete; Shojaolsadati, Paria; Uzuner, Kubilay; Donmez, Dilek Burukoglu; Kanbak, Gungor; Tıbbi Biyokimya / Medical Biochemistry
    Boric acid and omega-3 are used as essential elements for both animal and human health. Many researchers have shown these beneficial effects on cardiac and inflammatory markers. This study aims to evaluate cardiac protective effect of boric acid and omega-3 against MI (myocardial infarction), probably due to the suppression of pro-inflammatory cytokines of natriuretic peptides in rats. Fifty male Sprague-Dawley rats were randomly divided into five groups: control, MI, MI+boric acid, MI+omega-3, and MI+boric acid+omega-3. Saline solution (2 ml/day), omega-3 (800 mg/kg/day), and boric acid (100 mg/kg/day)+omega-3 (800 mg/kg/day) were orally administered to the relevant groups throughout the 28 days. To constitute the MI model, the rats were exposed to isoproterenol-HCl (ISO) (200 mg/kg, S.C.) on the 27th and 28th. In the MI group, serum levels of CK-MB, BNP, and TNF-alpha are increased significantly. Also, ST waves and heart rates were higher in the MI than the control. These results demonstrate that biochemical results healed in MI+boric acid, MI+omega-3, and MI+boric acid+omega-3 groups compared MI group. ECG and light microscope results supported the findings as well. The statistical analysis showed that boric acid and/or omega-3 has protective effects on cellular damage in MI.
  • Thumbnail Image
    Article
    Citation Count: 3
    Hepatotoxicity and nephrotoxicity following long-term prenatal exposure of paracetamol in the neonatal rat: is betaine protective?
    (Walter de Gruyter Gmbh, 2020) Ozkoc, Mete; Karimkhani, Hadi; Kanbak, Gungor; Donmez, Dilek Burukoglu; Tıbbi Biyokimya / Medical Biochemistry
    Background: Paracetamol is one of the widely used antipyretic and analgesic drug around the world. Many researchers showed that paracetamol caused to hepato-toxicity or nephrotoxicity. Objective: In the present study, we aimed to determine whether betaine has protective effects on hepatotoxicity and nephrotoxicity in neonate rats, following to long term maternal paracetamol exposure. Materials and methods: Randomly chosen neonates, from the neonate pools, were divided into three groups; Control (n=13), APAP (n=13), and APAP + Betaine (n=13). Physiological saline, paracetamol (30 mg/kg/day), and paracetamol (30 mg/kg/day) + betaine (800 mg/kg/day) were orally administered to the relevant groups during the pregnancy period (approximately 21 day). Following to the birth, neonates were decapitated under anaesthesia and tissue samples were taken for biochemical and histological analyses. Results: The statistical analysis showed that, malondialdehyde and nitric oxide levels increase significantly in APAP group, while paraoxonase, arylesterase activity and glutathione levels decrease. After the betaine administration, glutathione levels, paraoxonase and arylesterase activities increased while malondialdehyde and nitric oxide levels decreased in APAP + betaine group. These biochemical findings also were supported by histological results. Conclusion: In this study, our biochemical and histological findings indicate that betaine can protect the tissue injury caused by paracetamol.