Silver nanoparticles (Ag NPs) have unique properties and display an important role in bioactivities such as antimicrobial, antiviral, antifungal, and anticancer. Stable Ag NPs were prepared by reaction of silver nitrate solution with extract of Melissa and characterized by UV-Vis spectroscopy, AFM, SEM, XRD, and Zeta potential. The resulted Ag NPs have a size range between 20 and 35 nm. The current study aims to evaluate the gastroprotective effect of Ag NPs against ethanol-induced gastric ulcers in rats. Thirty rats were randomly divided into five groups. The experimental groups were fed 175 and 350 ppm/p.o of Ag NPs orally. Ag NPs improved the adversative influence of ethanol-induced stomach damage as confirmed by declining ulcer index and raised the percentage of ulcer prevention. Significantly reduced ethanol-induced gastric lesions were evidenced by increased mucus secretion and pH of stomach content, decreased ulcer area, nonappearance of edema, and leucocyte penetration of the subcutaneous layer. In gastric homogenate, Ag NPs displayed a substantial upsurge in superoxide dismutase (SOD), catalase (CAT) activities, and significantly reduced malondialdehyde (MDA) levels., Ag NPs increased the intensity of periodic acid Schiff stained (PAS) and produced over-regulation of HSP-70 and down-regulation of Bax proteins. Ag NPs confirmed gastro-protection which might be attributed to its antioxidant effect, increased mucus secretion, increased SOD, and CAT, reduced MDA level, over-regulation of HSP-70 protein, and down-regulation of Bax protein.

The study in vivo assessed the effect of pinostrobin on the histology, immunohistochemistry, and biochemical parameters of thioacetamide (TAA) induced liver cirrhosis in Sprague Dawley rats. The rats were noticeably gavaged with two doses of pinostrobin (30 mg/kg and 60 mg/kg) with TAA and exhibited a substantial decrease in the liver index and hepatocyte propagation with much minor cell injury. These groups meaningfully down-regulated the proliferation of cellular nucleus antigen (PCNA) and alpha-smooth muscle actin (α-SMA). The liver homogenate displayed augmented antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activities escorted with reducing in malondialdehyde (MDA) level. The serum level of bilirubin, total protein, albumin, and liver enzymes (ALP, ALT, and AST) returned to normal and was similar to that of normal control and silymarin with TAA-treated groups. pinostrobin-fed groups also decreased the level of Tumor necrosis factor-alpha (TNF-α), Interleukin-6 (IL-6), and increased the level of Interleukin-10 (IL-10). Acute toxicity with a higher dose of 500 mg/kg of pinostrobin did not manifest any toxicological signs in rats. The hepatoprotective effect of pinostrobin could be due to potentially inhibited the progression of liver cirrhosis, down-regulation of PCNA and α-SMA proliferation, prevented oxidation of hepatocytes, improved SOD and CAT enzymes, condensed MDA, repairs of liver biomarkers, reduced cellular inflammation and modulation of inflammatory cytokines.

This research in vivo assessed the impact of the ethanolic extract of Annona muricata (A. muricata) on the histopathology, immunohistochemistry, and biochemistry of thioacetamide (TAA)-induced liver cirrhosis in Sprague Dawley rats. The rats, gavaged precisely with two doses of A. muricata (250 mg/kg and 500 mg/kg) with TAA, presented a substantial reduction in the liver index and hepatocyte propagation, with much lower cell injury. These groups showed meaningfully down-regulated proliferating cell nuclear antigen (PCNA) in the liver and spleen, α-smooth muscle actin (α-SMA), and transforming growth factor-beta 1 (TGF-β1) in liver parenchymal tissue. The liver homogenate displayed enhanced antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activity, along with a decrease in malondialdehyde (MDA) levels. The serum levels of bilirubin, total protein, albumin, and liver enzymes alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were returned to normal and were similar to that of the normal control and silymarin with TAA-treated groups. Oral acute toxicity revealed no evidence of any toxic symbols or mortality in rats, indicating the safety of A. muricata. Therefore, the normal microanatomy of hepatocytes, the clampdown of PCNA, α-SMA, TGF-β, improved antioxidant enzymes (SOD and CAT), and condensed MDA with repairs of liver biomarkers validate the hepatoprotective effect of A. muricata.

The protective effect of biochanin A (BCA) on the histopathology, immunohistochemistry, and biochemistry of thioacetamide (TAA)-induced liver cirrhosis in vivo was investigated. There was a significant reduction in liver weight and hepatocyte propagation, with much lower cell injury in rat groups treated with BCA (25 mg/kg and 50 mg/kg) following a TAA induction. These groups had significantly lower levels of proliferating cell nuclear antigen (PCNA) and α-smooth muscle actin (α-SMA). The liver homogenates showed increased antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as decreased malondialdehyde (MDA) levels. The serum biomarkers associated with liver function, namely alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyl transaminase (GGT), returned to normal levels, comparable to those observed in both the normal control group and the reference control group. Taken together, the normal microanatomy of hepatocytes, the inhibition of PCNA and α-SMA, improved antioxidant enzymes (SOD, CAT, and GPx), and condensed MDA with repairs of liver biomarkers validated BCA’s hepatoprotective effect.

Alpinetin is an original medicinal plant flavonoid derived from Alpinia katsumadai and has several biological activities. The current research aimed to evaluate the hepatoprotective effects of Alpinetin against thioacetamide (TAA)-induced liver cirrhosis in rats. Five groups of rats were utilized in this study. Hepatic injury was measured macroscopically and microscopically for entire groups. The rats’ body weight was significantly lower in the TAA control group, likened to rats fed with Silymarin or Alpinetin groups, while liver weight was significantly greater in the TAA control group when equated to rats nourished with Alpinetin groups. A histopathological investigation of hepatic tissues displayed that TAA remarkably induced hepatocyte necrosis and gristly connective tissue propagation in the TAA control group. Alpinetin implicitly decreased the influence of TAA toxicity and diminished fibrosis of liver tissues. The TAA control group presented an increase in liver enzymes (ALP, ALT, and AST) and a decrease in total protein and albumin. Rats who were fed Alpinetin had significantly lower hepatic enzyme activity as well as augmented total protein and albumin, yet they were close to the normal range. Superoxide dismutase (SOD) and Catalase (CAT) enzymes in hepatic homogenate were significantly reduced, and malondialdehyde (MDA) was meaningfully elevated in the TAA control group, while rats fed with Alpinetin had significantly increased SOD and CAT achievement and depressed MDA level. Alpinetin-gavaged groups had reduced levels of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6), significantly down-regulated Proliferating cell nuclear antigen (PCNA), Alpha-smooth muscle (α-SMA), and reduced hepatic stellate cell activity. However, the TAA control group significantly up-regulated PCNA and α-SMA and increased the activity of hepatic stellate cells. Alpinetin was nontoxic and could improve defensive mechanisms against hepatic tissue injury. Acute toxicity tests discovered no evidence of any toxic signs or dead rats, which highlights the safety of Alpinetin. Consequently, the investigation´s outcomes revealed that the hepatoprotective effects of Alpinetin in TAA-induced hepatic impairment might be due to reduced TAA toxicity, increased protein and albumin, increased SOD and CAT levels, reduced MDA levels, and modulation of inflammatory cytokines and their anti-oxidant activities, and suppressed PCNA and α-SMA.

Synthesis of gold nanoparticles exhibition wide range of bioactivities and was conventionally used for the remedy of numerous disorders. Our study aims to measure the gastroprotective effect of synthesized gold nanoparticles on absolute ethanol-induced stomach ulceration in rats. The rats were noticeably administered with two doses of gold nanoparticles (175 ppm and 350 ppm) with absolute alcohol and showed a significant improvement in the adverse effect of ethanol-produced stomach damage as confirmed by decreasing ulcer index and raising % of ulcer prevention. Increased mucus pH of stomach content reduced ulcerated portion, condensed or nonappearance of edema, and white blood cells permeation subcutaneous layer. In gastric tissue homogenate, synthesized gold nanoparticles presented a substantial increase in superoxide dismutase (SOD), catalase (CAT) actions, and a substantial lessening of malondialdehyde (MDA) amount. Besides, gold nanoparticle increases the intensity of periodic acid Schiff stained (PAS) of the gastric epithelium of the stomach. Gold nanoparticles confirmed gastro-protective effects which might be qualified to its antioxidant, increase mucus secretion, increase endogenous enzymes (SOD and CAT), and reduce MDA quantity.