ArticleMolecular medicine reports2017
Pien Tze Huang Gan Bao attenuates carbon tetrachloride‑induced hepatocyte apoptosis in rats, associated with suppression of p53 activation and oxidative stress.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Antioxidant Properties Mediate Nephroprotective and Hepatoprotective Activity of Essential Oil and Hydro-Alcoholic Extract of the High-Altitude PlantAntioxidants (Basel, Switzerland) · 2023Article
- Prophylactic and curative effects of Carica papaya Linn. pulp extract against carbon tetrachloride-induced hepatotoxicity in male rats.Environmental science and pollution research international · 2023Article
- Pien-tze-huang promotes wound healing in streptozotocin-induced diabetes models associated with improving oxidative stressFrontiers in pharmacology · 2023Article
- Identification of circular RNA biomarkers for Pien Tze Huang treatment of CCl4‑induced liver fibrosis using RNA‑sequencing.Molecular medicine reports · 2022Article
- Protective effects of Longhu Rendan on chronic liver injury and fibrosis in mice.Liver research (Beijing, China) · 2022Article
- The antioxidant and anti-inflammatory effects of Carica Papaya Linn. seeds extract on CClBMC complementary medicine and therapies · 2021Article
- The Effect of Infertility on the Liver Structure, Endocrinology, and Gene Network in Japanese Flounder.Animals : an open access journal from MDPI · 2021Article
- Pien Tze Huang (PZH) as a Multifunction Medicinal Agent in Traditional Chinese Medicine (TCM): a review on cellular, molecular and physiological mechanisms.Cancer cell international · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pien Tze Huang Gan Bao (PZH‑GB), a traditional Chinese medicine, has been used for thousands of years as a protective remedy effective against liver injury induced by excessive alcohol and smoking. The present study aimed to evaluate the protective effects and potential mechanisms of PZH‑GB against carbon tetrachloride (CCl4)‑induced hepatic injury. Rats were pre‑treated with silymarin (50 mg/kg) or different doses of PZH‑GB (150, 300 or 600 mg/kg) orally administered for 7 days. At the end of treatment, the rats were intraperitoneally injected with CCl4, or control rats received a corn oil injection. The lactate dehydrogenase (LDH) levels in serum were evaluated. Apoptosis was assessed via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. p53, B‑cell lymphoma 2 (Bcl‑2), B cell‑lymphoma 2‑associated X protein (Bax), cyclooxygenase‑2 (COX‑2), inducible nitric oxide synthase (iNOS) and cytochrome P450 family 2 subfamily E member 1 (CYP2E1) were measured by reverse transcription‑quantitative polymerase chain reaction and western blotting. The activity of caspase‑9 and caspase‑3 were measured by a colorimetric assay. The results indicated that silymarin and PZH‑GB prevented CCl4‑induced serum LDH elevations, and CCl4 induced high levels of LDH. Compared with the CCl4 group, silymarin and PZH‑GB treatment significantly decreased LDH levels. Histopathological results revealed that silymarin and PZH‑GB ameliorated the CCl4‑induced liver histological alterations. The TUNEL results showed that compared with the control group, CCl4 induced liver cell apoptosis, while silymarin and PZH‑GB treatment inhibited apoptosis and the TUNEL‑positive cells. The elevated expression of Bax, p53, iNOS, COX‑2 and CYP2E1 were reduced by silymarin or PZH‑GB pretreatment, whereas reduced Bcl‑2 expression levels were increased. CCl4 increased the activity of caspase‑9 and ‑3 by 6.86‑ and 7.42‑fold, respectively; however, silymarin and PZH‑GB ameliorated this effect. In conclusion, silymarin and PZH‑GB treatment prevented the deleterious effects on liver functions by attenuation of oxidative stress, inflammation and mitochondrial apoptosis via the p53 signaling pathway.
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