A combination extract of kaffir lime, galangal, and lemongrass maintains blood lipid profiles, hepatocytes, and liver mitochondria in rats with nonalcoholic steatohepatitis

Tirawanchai, Napatara; Kengkoom, Kanchana; Isarangkul, Duangnate; Burana-osot, Jankana; Kanjanapruthipong, Tapanee; Chantip, Surachai; Phattanawasin, Panadda; Sotanaphun, Uthai; Ampawong, Sumate

doi:10.1016/j.biopha.2020.109843

Cited by 15 publications

(10 citation statements)

References 37 publications

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“…A change in the metabolic energy source under diabetic conditions results in increased oxygen consumption in the kidney and leads to renal hypoxia, ischaemia and necrosis [8,32]. Our recent studies have demonstrated that cellular power synthesis (Haloacid Dehalogenase-Like Hydrolase Domain-Containing [HDHD]-3) and a mitochondrial apoptotic marker (NADH: ubiquinone oxidoreductase core subunit S1 [NDUFS-1]) in liver mitochondria in sericin-fed rats are preserved compared to those of non-treated rats under hypercholesterolemic conditions [38,39]. In this study, the immunogold labelling technique indicates signi cant upregulation of HDHD-3 and NDUFS-1 in the alpha 2u-globulin nephropathic rats ( Figure 5).…”

Section: Discussionmentioning

confidence: 99%

“…These sections were then stained with haematoxylin and eosin (H&E) and examined under a light microscope, focusing on (i) intracytoplasmic hyaline droplet deposition, tubular cast formation, tubular degeneration, tubular regeneration and Bowman's space distension with proteinaceous uid deposition for kidney, (ii) pyknotic nuclei, lymphocyte in ltration and centrilobular microvesicular steatosis for liver and (iii) Islet of Langerhans degeneration, vacuolar degeneration in the acinar gland and interstitial cell necrosis and in ammation of the pancreas. The lesions were semi-quantitatively graded using H-score (distribution [~0-100%/section] × severity score [0-3: 0 = absent, 1 = mild, 2 = moderate and 3 = severe]) as shown in our previous studies [39][40][41][42][43].…”

Section: Histopathological Studiesmentioning

confidence: 99%

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Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease

Kengkoom

Angkhasirisap

Kanjanapruthipong

et al. 2021

Preprint

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Background: Alpha-2u globulin nephropathy mainly shows toxicological pathology only in male rats induced by certain chemicals and drugs, such as levamisole (antiparasitic and anticancer drugs). Streptozotocin (STZ) is also an anticancer-antibiotic agent that has been used for decades to induce a diabetic kidney disease model in rodents. The purpose of this study is to determine if STZ causes alpha-2u globulin nephropathy in male rats during an advanced stage of diabetic kidney disease.Methods: To test this hypothesis, the present study used a male diabetic Wistar rat model with 45 mg/kg of STZ injected intraperitoneally. Hyperglycaemic rats were divided into 2 groups: with and without alpha-2u globulin deposition in proximal tubule. Alpha-2u globulin nephropathy was examined by histopathological and electron microscope studies. Water absorption and filtration capacities (via aquaporin [AQP]-1, -2, -4 and -5) and mitochondrial function (through haloacid dehalogenase-like hydrolase domain-containing protein [HDHD]-3 and NADH-ubiquinone oxidoreductase 75 kDa subunit [NDUFS]-1 proteins) were determined using immunohistochemistry, immunofluorescence and immunogold labelling techniques.Results: More than 80% of severe clinical illness rats induced by STZ injection simultaneously exhibited alpha-2u globulin nephropathy with mitochondrial degeneration and filtration apparatus especially pedicels impairment. They also showed significantly upregulated AQP-1, -2, -4 and -5, HDHD-3 and NDUFS-1 compared with those of the rats without alpha-2u globulin nephropathy.Conclusions: STZ-induced alpha-2u globulin nephropathy during diabetic kidney disease in association with deterioration of pedicels, renal tubular damage with adaptation and mitochondrial driven apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Histopathological Studiesmentioning

confidence: 99%

Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease

Kengkoom

Angkhasirisap

Kanjanapruthipong

et al. 2021

Preprint

Self Cite

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show abstract

“…A change in the metabolic energy source under diabetic conditions results in increased oxygen consumption in the kidney and leads to renal hypoxia, ischaemia and necrosis [8,29]. Our recent studies have demonstrated that cellular power synthesis (Haloacid Dehalogenase-Like Hydrolase Domain-Containing [HDHD]-3) and a mitochondrial apoptotic marker (NADH: ubiquinone oxidoreductase core subunit S1 [NDUFS-1]) in liver mitochondria in sericin-fed rats are preserved compared to those of non-treated rats under hypercholesterolemic conditions [35,36]. In this study, the immunogold labelling technique indicates significant upregulation of HDHD-3 and NDUFS-1 in the alpha 2u-globulin nephropathic rats (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…These sections were then stained with haematoxylin and eosin (H&E) and examined under alight microscope, focusing on (i) intracytoplasmic hyaline droplet deposition, tubular cast formation, tubular degeneration, tubular regeneration and glomerular atrophy for kidney, (ii) pyknotic nuclei, lymphocyte proliferation and centrilobular microvesicular steatosis for liver and (iii) Islet of Langerhans degeneration, vacuolar degeneration in the acinar gland and interstitial cell necrosis and inflammation of the pancreas. The lesions were semi-quantitatively graded using H-score (distribution [~0-100%/section] × severity score [0-3: 0 = absent, 1 = mild, 2 = moderate and 3 = severe]) asshown in our previous studies[36][37][38][39][40].…”

mentioning

confidence: 99%

Streptozotocin induces alpha-2u globulin nephropathy in male rats during the end-stage of diabetic kidney disease

Kengkoom¹,

Angkhasirisap²,

Kanjanapruthipong³

et al. 2020

Preprint

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Background Alpha-2u globulin nephropathy mainly shows toxicological pathology only in male rats induced by certain chemicals and drugs, such as levamisole (antiparasitic and anticancer drugs). Streptozotocin (STZ) is also an anticancer-antibiotic agent that has been used for decades to induce a diabetic kidney disease model in rodents. The purpose of this study is to determine if STZ causes alpha-2u globulin nephropathy in male rats during an advanced stage of diabetic kidney disease. Methods To prove this hypothesis, the present study used a male diabetic Wistar rat model with 45 mg/kg of STZ injected intraperitoneally. Hyperglycaemic rats were divided into 2 groups: with and without end-stage kidney disease. Alpha-2u globulin nephropathy was examined by histopathological and electron microscope studies. Water absorption and filtration capacities (via aquaporin [AQP]-1, -2, -4 and -5) and mitochondrial function (through haloacid dehalogenase-like hydrolase domain-containing protein [HDHD]-3 and NADH-ubiquinone oxidoreductase 75 kDa subunit [NDUFS]-1 proteins) were determined using immunohistochemistry, immunofluorescence and immunogold labelling techniques. Results More than 80% of end-stage diabetic kidney disease induced by STZ injection simultaneously exhibited alpha-2u globulin nephropathy with mitochondrial degeneration and filtration apparatus especially pedicels impairment. They also showed significantly upregulated AQP-1, -2, -4 and -5, HDHD-3 and NDUFS-1 compared with those of the rats without alpha-2u globulin nephropathy. Conclusions STZ-induced alpha-2u globulin nephropathy during end-stage diabetic kidney disease in association with deterioration of renal filtration, renal tubular damage with adaptation and mitochondrial apoptosis.

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“…[ 16–21 ] In addition, recent studies have reported that CT could also ameliorate the hepatotoxicity induced by a high‐cholesterol diet. [ 22 ] Yet, the effects of CT on DOX‐induced hepatotoxicity have not yet been investigated.…”

Section: Introductionmentioning

confidence: 99%

Citronellal ameliorates doxorubicin‐induced hepatotoxicity via antioxidative stress, antiapoptosis, and proangiogenesis in rats

Qiu

Liu

et al. 2020

J Biochem & Molecular Tox

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Doxorubicin (DOX) is a very effective broad‐spectrum anticancer drug, yet its clinical application is badly restricted due to its serious side effects. Citronellal (CT), a specialized metabolite of plants found in Cymbopogon spp., is proved to exhibit many beneficial properties. In the current study, we intended to investigate the effect of CT on DOX‐induced hepatotoxicity in rats. Rats were treated with CT (200 mg/kg b.w./day orally), and given DOX (2.5 mg/kg b.w./week, intraperitoneally) to induce hepatotoxicity for six consecutive weeks. The results showed that CT administration could attenuate the DOX‐induced pathological changes of liver tissues and ameliorated the inappropriate alteration of liver function biomarkers (serum glutamic aspartate aminotransferase, glutamic pyruvic transaminase, and albumin) in serum and oxidative stress parameters (malondialdehyde, superoxide dismutase, and reduced glutathione) in the liver. Moreover, CT mitigated the Bax/Bcl‐2 ratio and caspase‐3 expression to inhibit cell apoptosis. Further study indicated that CT therapy could enhance the protein levels of p‐PI3K, p‐Akt, and CD31 in the liver. These results demonstrate that CT can ameliorate DOX‐induced hepatotoxicity in rats mediated by antioxidative stress, antiapoptosis, and proangiogenesis.

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A combination extract of kaffir lime, galangal, and lemongrass maintains blood lipid profiles, hepatocytes, and liver mitochondria in rats with nonalcoholic steatohepatitis

Cited by 15 publications

References 37 publications

Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease

Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease

Streptozotocin induces alpha-2u globulin nephropathy in male rats during the end-stage of diabetic kidney disease

Citronellal ameliorates doxorubicin‐induced hepatotoxicity via antioxidative stress, antiapoptosis, and proangiogenesis in rats

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